NEUR1020

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Final Exam

Last updated 10:42 PM on 6/15/26
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104 Terms

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Testability

Does the theory generate hypotheses that can be evaluated against data?

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Falsifiability

Are there potential observations, or patterns of data, that are disallowed by the theory?

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Paradigm

A framework for understanding and investigating phenomena with a discipline.

Defines concepts that are used in theories, research questions that are addressed by a discipline, and methodologies used to investigate these questions.

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Origins of the Behaviourist Paradigm

Freud urged us to ‘look inward’ and consider how the unconscious mind influenced our thoughts and behaviour. Behaviouristst encouraged us to consider how the external environment shapes our thoughts and behaviours.

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Watson’s Methodological Behaviourism

Rejected the study of unobserved phenomena (such as overt behaviours) could be studied scientifically.

Prompted a shift in focusing on relationships between publicly observable stimuli and the behavioural consequences.

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Skinner’s Radical Behaviourism

Broadened the definition of ‘behaviour’ to include ‘private’ events (e.g., thoughts and feelings) as legitimate scientfic topics of study.

Argued that the external environment was the determinant of both observable and unobservable behaviours.

Mental events, therefore, are not causes of behaviour, but are themselves behaviours caused by the environment.

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Cognitive Paradigm

Framework focusing on internal mental processes

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Biological Paradigm

A theoretical framework in psychology that explains human behaviour, personality, and mental disorders through physical factors (including genetics, neurochemistry and brain structure.

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Features of a Science

Grounded in observation. Science is cumulative. Self-correcting. Achieves explanation and understanding.

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Behavioural Paradigm

A psychological framework focusing on observable, measurable behaviours rather than internal mental processes.

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Control (Least to Most)

Introspection, Natural Observation, Case History, Surveys, Correlational Designs, Experiments.

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The Stroop Effect

Refers to the phenomenon where individuals take longer to name the colour of ink that the names of colours are written in than it does to read the colour names.

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Cerebrum (Cerebral Hemispheres)

Two hemispheres divided by longitudinal fissure or inter-hemispheric fissure

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Cerebral Cortex

Outermost surface layer of the cerebrum.

Grey Matter (Surface of the brain 2-4mm thick, highly folded to maximise surface area)

White Matter (underneath grey matter is all “wiring” such as axons of teh neurons connecting to the spinal cord and to other areas of the cortext)

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Frontal Lobe

Primary Motor Cortex

Premoteor Area

Motor Speech Area

Prefrontal Area

Executive functions (reasoning, planning, problem-solving, inhibitory control, working memory)

Motor functions (premotor - motor planning, cortex - execution)

Speech Production (Broca’s area)

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Parietal Lobe

Primary Somatosensory Cortex (perception of touch)

Sense of space and locations (gives sense of stable world around us relative to body position)

Spatial attention (directing attention and eye movements to explore the visual world)

Linking vision to action (represents spatial location of objects around us for guiding actions)

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Occipital Lobe

Primary Visual Cortex (V1) - all visual perception

Higher visual areas - different regions process shape, colour, orientation and motion

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Temporal Lobe

Primary auditory cortex (perception of sound)

Language comprehension, Wernicke’s area)

Medial Temporal Lobe (Limbic system, amygdala and hippocampus)

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Limbic System

Amygdala - Fear and arousal, responds to threats/danger, fear/learning phobias

Hippocampus - learning and memory, forming new episodic memories, damage causes anterograde amnesia (can’t form new memories)

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Corpus Callosum

Neuron connections between the left and right hemispheres and allows communication between hemispheres

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Broca’s Area

Speech production

1861 Paul Broca described a patient who was unable to speak after damage to the left frontal lobe

Speech is slow and non-fluent

Difficulty finding appropriate words (anomia)

Speech still caries meaning, comprehension is mostly unaffected

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Wernicke’s Area

Language comprehension

1874 Carl Wenicke suggested that lesions to the left posterior temporal lobe led to deficits in language comprehension

Unable to understand language, deficit in comprehension

Speech is fluent with normal prosody (rhythm, intonation)

Speech has no meaning

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Wilder Penfield

Stimulated the brain with electrical probes while the patients were conscious, during surgery for epilepsy

1951 published maps of motor and sensory cortices of the human brain

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Homunculus

Primary sensory cortex and Primary motor cortex

Brain function “mapped” by electrical stimulation, brain stimulation leads to sensation or movement

Size of area on cortex determines sensitivity or five motor control

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Nervous System Break Down

CNS (Brain and spinal cord) and PNS

PNS - Autonomic (involuntary) Somatic (voluntary, sensory and motor)

Autonomic - Sympathetic (emotional arousal, stress, fear, fight or flight response, increases heat-rate, respiration, perspiration, pupils dilate) and Parasympatheic (rest and digest, lowers heart-rate, respiration, increases stomach and intenstine activity)

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Brain Stem

Medulla

Autonomic nervous system functions

Controls heart rate, respiration, regulation of blood pressure, body temperature

Reflex centres for coughing, sneezing, swallowing, vomiting

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Persistent Vegetative State

Severe damage to upper brain

If brain stem is not damaged, autonomic nervous system functions can remain

Sometimes normal respiration, control of heart rate, and some face and eye movements remain

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Locked-In Syndrome

Amyotrophic Lateral Sclerosis (ALS) or Motor Neuron Disease (MND)

Brain Injury

Intact cerebrum and brain stem but disconnected from spinal cord

Normal cognitove function, vision, and hearing but mostly cannot move

Patients may be fully conscious and aware but totally unresponsive

Pateints apprea the same as those with persistent vegetative state

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High to Low level function

Cerebral Hemispheres - Cortex, planning, reasoning, problem-solving (frontal lobe), language and perception

Brainstem - Autonomic nervous system functions (heart-rate, respiration, blood pressure)

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Cerebellum

Hindbrain

Sense of balance and co-ordination of complex movement

Motor-learning - fine adjustment of movement based on feedback

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Glial Cells

Oligodendrocytes - Produce the myelin sheath that wraps around axons

Astrocytes - Supply nutrients from blood to the neurons, maintain “blood-brain barrier”

Microglia - brain’s immune system, clean up foreign of toxic substances

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The Myelin of Axons

Oligodendrocytes from myelin sheath by wrapping around the axon

Essential for efficient communication, for propagation of signals along axon

Multiple sclerosis involves loss of myelin, disrpution of efficient neurl communication throughout the body

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Neural signals go one way

Pre-synaptic: before the synapse, from cell body to axon terminal

Post-synaptic: after the synapses, from dendrite to the cell body

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Neurons Electrical Signals

Electrical signal “pulse” travels along the axon

Fixed size - either on or off, signal or no-signal (not large or small)

<p>Electrical signal “pulse” travels along the axon</p><p>Fixed size - either on or off, signal or no-signal (not large or small) </p>
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Membrane Potential

The electrical voltage difference between the inside and outside of a biological cell

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Resting Potential

The stable electrical charge difference across the cell membrane of an excitable cell (neuron) when it is not actively transmitting signals

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Action potential

A rapid, temporary reversal of electrical charge across the membrane of an excitable cell

Depolarisation/repolarisation is fact (occurs in less than 0.002 seconds)

Repolarisation undershoots - (refractory period - more difficult for another action potential to occur), further to threshold to trigger another action potential

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Cell Membrane Wall

70% of the brain is water with water surrounding (extra-cellular) and filling (intra-cellular) cells

Cell membrane forms barrier between extra-cellular and intra-cellular fluid

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Ions and Electrical Potential across Cell Membrane

Sodium (Na+) and Potassium (K+) positively charged ions

Different concentrations outside and inside cell, across cell membrane

Gives difference in electrical charge (potential) across cell membrane

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Ion Channels in Cell Membrane

Open and close to pass or block movement of ions across cell membrane

Ions move between intra and extra-cellular fluid

Movement of ions changes electrical potential

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Sodium Potassium Pump

Actively pumps Na+ and K+ across cell membrane

Overly pumps positive charge out of cell (3 Na+ out for every 2 K+ in)

Positive charge will naturally move towards negative area (opposites attract)

Maintains negative resting membrane potential (approx ~70mv)

Uses about 25% of body total energy (70% of brain energy)

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Voltage-Dependent Ion Channels

Voltage-dependent ion channel, closed at resting potential

Open when membrane potential reaches threshold voltage

Allows flow of ions across membrane

Positive ions (Na+) can flow from outside into the cell (because positive charge will naturally move towards negative area)

Causes depolarisation of cell (voltage less negative = closer to 0)

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Depolarisation

Na+ channels open when voltage exceeds threshold

Na+ flows into the cell

Less negative potential

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Repolarisation

Na+ channels close and K+ channels open after depolarisation

K+ flows out of cell

Plus Na/K pump

More negative potential

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Synapses and Neural signals

Neurotransmitter release - depolarisation of axon terminal (action potential) triggers release of neurotransmitter which acts on receptor on post-synaptic neuron to open ion channels and pass signal

Synaptic vesicles - stores neurotransmitter in pre-synaptic terminal (recycled neurotransmitter taken back into pre-synaptic terminal is re-packaged into vesicles)

Re-uptake pump - clears neurotransmitter form synaptic cleft back into pre-synaptic terminal

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Dopamine - Parkinson’s Disease

Loss of dopamine in the basal ganglia deep in the brain

Primarily affects movement

Treatment with L-DOPA replaces the dopamine in the brain

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SSRI

Anti-depressant drug for serotonin

Selective Serotonin Re-uptake Inhibitors

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MAOIs

Anti-Depressant Drugs for serotonin

Monoamine Oxidase Inhibitors

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Sending Signals Neurotransmitter Release

Depolarisation of axon terminal triggers release of neurotransmitter

Neurotransmitter acts on receptor and post-synaptic neuron to open ion channels and pass signal

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Ligand Gates

Neurotransmitter receptors open ion channels when neurotransmitter binds

Different neurotransmitters bind to and open different ion channels (Na+, K+, Cl-) to change membrane potential in different ways

Receptor Binding - can cause depolarisation and hyperpolarisation

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Excitatory Post-Synaptic Potential

Receptor opens channels that cause depolarisation, closer to threshold for action potential

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Inhibitory Post-Synaptic Potential

Receptor opens channels that cause hyperpolarisation, further from threshold for action potential

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Graded Potentials

Excitatory and inhibitory inputs combine together which change the membrane potential on post synaptic cell

Depends on the strength of synapse connection (strong connection causes large change in membrane potential, weak connection causes small change)

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When do inputs trigger an action potential?

Membrane potential at axon hillock depends on sum and timing of inputs through dendrites

If enough excitatory inputs occur together close enough in time, membrane potential will exceed threshold level for action potential

If membrane potential exceeds threshold level (at axon hillock) it triggers action potentials and neuron fires

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Neuropsychology - Brain Lesions

Explains normal brain function by examining what changes when part of the brain is damaged (stroke or brain injury inhumans, induced lesions in animals from electrical or chemical stimuli)

Assumption is whatever changes in behaviour/cognition must rely on that part of the brain that is damaged

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Single Neuron Recording

Place a single thin electrode to an animals brain and record action potentions firing form a single neurons

Measures what the neuron encodes or detects

Best localisation and timing of brain function

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EEG - Electroencephalography

Summed activity from action potentials of neurons in the cortex cause electrical activity change on the scalp

Measure voltage changes from electrodes placed on the scalp

Wave forms vary with brain states

Constant oscillations and frequencies change with alertness and sleep

Clinical use - detecting stages of sleep, monitoring for epileptic seizures

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ERPs - Event-Related Potentials

Brain activity related to a specific event or stimulus

Average together >100 trials of EEg response to the stimulus

Peaks represent different stages of processing of the stimulus

Can show precise timing of information processing in the brain

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Face Processing N170

ERPs can show precise time of information processing in the brain

100ms viewing any stimuli (peak brain activity 100ms after seeing visual stimulus, early brain processing of general visual features)

170ms viewing faces (peak of brain activity 170ms after seeing face, brain processing for face-recognition in visual cortex)

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PET

Positron Emission Tomography

1980-late 90s

Uses radioactive substances injected into the blood stream

Used now to map neurotransmitters or receptors in the brain

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fMRI

Functional Magnetic Resonance Imaging

1992 to current

Masures changes in blood oxygen level (BOLD signal)

Studies brain function

Oxygen is carried in blood and delivered to active neurons

Change in blood oxygen level = change in brain activity

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Spreading Activation Model Theory

Neurons represent a specific concept

Share connections with neurons that represent related concepts

Activation of one neuron leads to spreading activation to related or connected neurons

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Neuroplasticity - With Experience

Sensory and motor cortex areas expand with use and experience

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Neuroplasticity - After Damage

No rehab - no movement, motor cortex gets small maladaptive plasticity

With rehab - movement training, motor cortex area for hand expanded and movement improved

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Neuroplasticity in Blind People

Brain activity in visual cortext while reading braille

Visual cortex change only in blind people, not sighted people reading braille

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Physiological Blind Spot

Point at which the optic nerve leaves your eye is called the optic dics

At the top of the disc there can be no photoreceptors so you are blind to images that project to that position on your retinae

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Visual Signals

knowt flashcard image
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Left Hemisphere Lateralised Function

Language and Speech

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Right Hemisphere Lateralised Function

Tone of voice, face perception, perceptual grouping

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Contralateral Functions

Movement, sensation and visoin

Left Hemisphere - right body movement, sensation and vision

Right Hemisphere - left body movement, sensation and vision

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Language Left Hemisphere

Language comprehension, speech, reading and speech production

Language and hand dominance, no overall dominant hemisphere

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Corpus Callosum

Connects left and right hemisphere

Axons of neurons crossing to the opposite hemisphere

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Inter-Hemisphere Communication

Vision goes to contralateral hemisphere (left of screen → right hemisphere)

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Split Brain (Severed Corpus Callosum)

Last resort surgical treatment for very severe epilepsy to stop seizure activity from spreading to the other hemisphere

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Transduction

The conversion of electromagnetic radiation into neural events

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Coloured Aftereffects

Brain causes you to see things that are not present on the retinae

After protracted viewing of certain colours, you can see opppositely coloured after images

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Face Aftereffects

Perceptual illusions where prolonged viewing a face causes subsequent faces to appear distorted in the opposite direction

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What causes after effects

Occur because the firing rates of neurons that are responsive to an input adapt over time which means they become less responsive

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Response Selectivity in the Human Retinae

The ability of retinal ganglion cells to respond preferentially to specific visual features (such as direction of motion, edge orientation, or colour) rather than simply registering light intensity

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V1 Response Selectivity

Simple V1 cells are responsive to oriented stripes of contrast located in a specific subfield of its receptive field

End-stopped V1 cells are responsive to oriented stripes of contrast of a specific (limited) length

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Retinotopic Map

Adjacent neurons in visual brain regions encode information from adjacent regions on the retinal surface

Retinotopic mapping is most apparent in lower-level visual brain structures where neurons are associated with small receptive fields

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Lateral Geniculate Nucleus (LGN)

A key thalamic structure acting as the primary relay station for visual information between the retina and the primary visual cortex

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Primary Visual Pathway

Main route for conscious vision, transmitting retinal information via the LGN to the primary visual cortex (V1) for detail and colour processing

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Secondary Visual Pathway

Involves areas like V2-V5 and subcortical structures handling higher-order processing like motion, depth, and spatial awareness

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V1-V5

V1 - Primary visual cortex

V2 - Secondary visual cortex

V3 - Third visual area (processing dynamic form)

V4 - Fourth visual area (involved in color perception and shape recognition)

V5 - Middle Temporal Area (specialised motor detection, react to the direction and speed of movement)

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Cerebral Achromatopisa

Rare, acquired form of colour blindness due to damage of the V4 cortex (black and white vision)

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Prosopagnosia

Face blindness (Occiputal face area)

Adjacent to V1 and V4

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Cerebral Akinetopsia

Rare neuropsychological disorder where patients lose the ability to perceive visual motion, even though their eyesight and ability to see stationary objects remain normal

Damage to V5

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Limbic System

Hippocampus - medial temporal lobe, memory (forming new episodic memory and damage causes memory loss in the form of not being able to retain new memories), spatial navigation

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Top-Down

Cognitive control or volitional choice

Modulation by prior knowledge and experience

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Bottom-Up

Driven by external stimuli or unconscious states

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Spatial Neglect

Lesion to one hemisphere (frontal or parietal)

Commonly caused by a stroke

Deficit in directing to one side of space

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Fronto-Temporal Dementia (FTD)

Degeneration of neurons in frontal and temporal lobe

Symptoms

  • inappropriate actions (aggressive, sexual, or lack of care)

  • Apathy

  • Loss of empathy

  • Deficits in executive function

  • Speech, language and motor deficits


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Extinction (Classical Conditioning)

CR response will reduce in strength and disappear if the CS is repeatedly presented without the UCS

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Spontaneous recovery

Sudden reemergence of a previously extinguished conditioned response after a period of rest or delay

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Generalisation

Tendency for CR to appear with similar stimuli to CS

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Discrimination

Learned ability to differentiate between a CS and US

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Multi-Store Model of Memory

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Capacity of Sensory Memory

Nearly unlimited capacity but brief duration if not encoded into short-term memory

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Capacity of Short-Term Memory

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