Irina lectures

Question 1

What are the two major visual streams?

Answer 1

o Dorsal stream

o Ventral stream

Question 2

How many visual areas are arranged along the two major visual streams?

Answer 2

• 30+ visual areas arranged along two major pathways

Question 3

What is the role of the dorsal stream? Describe who postulated those roles and their evidence base.

Answer 3

 Processes “where” (computes spatial location)
• Ungerleider and Mishkin 1982
o If lesioned dorsal stream, monkeys unable to perform tasks that relied on spatial location perception
o Spatial perception
o Vision for action
 Processes “how” (uses vision to guide action)
• Goodale and Milner 1992
o Neuropsychological patients had difficulty reaching out to particular locations in space
• Strong interactions with motor system

Question 4

Where is the dorsal stream of visual information located?

Answer 4

 From primary visual cortex (V1) to posterior parietal lobe (occipito-parietal)

Question 5

Can the dorsal stream of visual information operate in an unconscious manner?

Answer 5

 Can operate in unconscious manner

Question 6

Where is the ventral stream of visual information located?

Answer 6

o Ventral stream-

 From primary visual cortex (V1) to inferior temporal cortex (occipito-temporal)

Question 7

What is the role of the ventral stream of visual information? Describe the evidence base

Answer 7

 Processes “what” (computes shape and object identity
• Ventral stream specialised for object perception and recognition
• Vision for recognition
 Contributes to conscious perception and awareness
 Ungerleider and Mishkin 1982
• Monkeys with lesions to ventral stream cannot learn shape associations with rewards
 Goodale and Milner 1992
• Neuropsychological patients with lesions in ventral stream have trouble identifying shapes and objects

Question 8

Does the dorsal stream of visual information operate in an unconscious manner?

Answer 8

 Important for conscious perception and awareness

Question 9

How many types of dorsal visual stream exist? Explain their role and location

Answer 9

• Two theories of two visual pathway
o Ungerleider and Mishkin (What/where)
 Functional characterisation of streams in terms of information content
o Milner and Goodale (perception vs action)
 Functional characterisation of streams in terms of process
o Recent evidence suggests that both these theories are correct and co-exist: in fact, 3 dorsal streams continue beyond posterior parietal cortex (3 types of dorsal streams exist instead of 1)
 Projects to prefrontal cortex, involved in spatial working memory- “where”
 Projects to premotor cortex, involved in action- “how”
 Projects to medial temporal lobe (hippocampal and parahippocampal gyrus), involved in navigation- “where” on an environmental scale

Question 10

Where are the primary visual areas situated?

Answer 10

• Primary visual areas- situated in back of occipital lobe

Question 11

Where are the intermediate visual areas situated?

Answer 11

• Intermediate visual areas- situated just outside the primary visual cortex

Question 12

Where are the higher order visual areas situated?

Answer 12

• Higher order visual areas- situated more anteriorly in the brain (inferotemporal cortex)

Question 13

Describe what neurons that belong to the early visual cortices respond to, their receptive field size and the organisation of these cortices

Answer 13

• Early visual areas (e.g. V1 and V2)
o Neurons respond to simple edges and points of light
 Respond to simple information
o Small receptive fields (0.1o-2o of visual angle)
 Neurons only respond if a preferred stimulus is placed in a specific part of the visual field
 Retinotopically organised cortex
 Early retinotopic cortex activated more by textures and scrambled objects

Question 14

Describe what neurons that
belong to the intermediate visual cortices respond to, their receptive field size and the organisation of these cortices

Answer 14

• Intermediate areas (e.g V4, TEO)
o Neurons respond to moderately complex features
 Combinations of edges, simple shapes, combinations of shapes and textures…
o Larger receptive fields (4-10o) of visual angle
 But restricted to one visual quadrant

Question 15

Describe what neurons that

belong to the higher-level visual cortices respond to, their receptive field size and the organisation of these cortices

Answer 15

•	High-level areas (e.g. IT)
o	Neurons respond to complex objects
	E.g. faces, hands, common objects
	Even individuals within a category
o	Very large receptive fields
	No retinotopic organisation, although there is preferential hemispheric responses

Question 16

Describe the hierarchical organisation of the ventral stream for humans vs monkeys

Answer 16

o Similar hierarchical organisation from parts to whole objects across the ventral stream compared to monkeys
 Corresponding areas of monkeys in humans are pulled further back and are more ventral

Question 17

In humans, what is the lateral occipital complex activated by?

Answer 17

 A more anterior area-LOC (lateral occipital complex)-activated more by full objects
• Preferentially activated by objects more than textures

Question 18

What are the two divisions of the lateral occipital complex?

Answer 18

• LOC has two divisions:
o Lateral surface of occipital lobe (usually termed LO)
o Ventral surace of occipital and temporal lobes (uusually termed VOT)

Question 19

Is the transition from part-based to full objects along the posterior-to-anterior axis of the ventral stream sudden or gradual?

Answer 19

 The transition from part-based to full objects is gradual along a posterior-to-anterior axis

Question 20

Why are tests designed to examine visual perceptual awareness needed?

Answer 20

 Dissociating responses due to perceptual awareness from those due to visual stimulation is difficult

Question 21

What are two different tests designed to examine visual perceptual awareness only?

Answer 21

o Binocular rivalry displays

o Noisy stimuli

Question 22

Describe how the binocular rivalry display visual perceptual awareness test is conducted and its results

Answer 22

o Binocular rivalry displays- visual input stays the same, but percept flips from one to another
 Each eye should get a differing percept but the visual stimulation should stay the same
• E.g presenting a superimposed stimulus and putting a different colour lens in front of each eye, so that each eye perceives a differing part of the stimulus
 This causes alternation between different stimuli (alternation rate approximately 4 seconds)

Question 23

Describe how the noisy stimuli visual perceptual awareness test is conducted

Answer 23

o Noisy stimuli
 Make the image fuzzier than clearer
 Titrating the stimulus to make it become more and more clear can allow measurement of the point where stimulus becomes a recognisable object

Question 24

What are two sources of evidence for hierarchy of conscious awareness in the ventral stream?

Answer 24

 Monkey neural recordings

 Human fMRI studies

Question 25

In monkey neural recordings, what % of V1/V2 neurons show correlation between activity and perceptual experience of the monkey? What does this demonstrate?

Answer 25

o Only 20% of V1/V2 neurons show correlation between activity and perceptual experience of the monkey  Primary visual cortices do not really correlate between activity and perceptual experience of the monkey

Question 26

In monkey neural recordings, what % of V4 neurons show correlation between activity and perceptual experience of the monkey? What does this demonstrate?

Answer 26

o About 40% of V4 neurons show correlation with perceptual experience- but often negative  There is a start of perceptual experience correlation, but it is not very tightly linked

Question 27

In monkey neural recordings, what % of IT neurons show correlation between activity and perceptual experience of the monkey? What does this demonstrate?

Answer 27

o About 90% of IT neurons show correlation with perceptual experience

Question 28

What part of the visual stream exactly is correlated to recognition performance? Are other visual areas also correlated to this recognition performance? Where is this effect the strongest?

Answer 28

o V1, V2 and V4 and lateral LOC are not differentially activated by identified vs unidentified stimuli o vOT activity correlates with recognition performance, rather than presence of stimulus o In vOT, correlation with recognition is stronger in more anterior parts (e.g. anterior fusiform gyrus)

Question 29

Where is the fusiform face area and what does it respond to preferentially?

Answer 29

``` o FFA (Fusiform Face Area) located in fusiform gyrus  Responds preferentially to faces compared to other objects ```

Question 30

Where is the parahippocampal place area and what does it respond to preferentially?

Answer 30

``` o PPA (Parahippocampal place area) located in the parahippocampal gyrus  Responds preferentially to buildings and place scenes compared to objects or faces ```

Question 31

Where is the extrastriate body area and what does it respond to preferentially?

Answer 31

``` o EBA (extrastriate body area) located in right occipito-temporal cortex  Responds preferentially to body parts compared to inanimate objects ```

Question 32

Describe the evidence that fusiform face area preferentially activates to faces whilst parahippocampal place area preferentially responds to places

Answer 32

 Tong et al. (1998)- o Did a binocular rivalry paradigm with fMRI-> asked people to tell them when they saw the face vs the building  Did a yoked stimulus paradigm, in which the stimuli were shown separately every four seconds, as a control o Found that FFA was activated when faces were seen but PPA was activated when buildings were seen

Question 33

What are the three theories of why there is functional organisation in the ventral stream?

Answer 33

 Domain-specificity hypothesis (Kanwisher)  Processing requirements (Gauthier, Tarr)  Network requirements

Question 34

Describe Kanwisher's domain-specificity hypothesis for why there is functional organisation in the ventral stream and some examples of this hypothesis

Answer 34

o Anatomical modules in the brain specialised for different evolutionarily important categories  Fusiform Face Area= faces  Parahippocampal place area= places/scenes  Extrastriate body area= bodies  Visual word form area (VWFA)= letters and words  Other ventral stream regions= little selectivity o Organisational principle is information content, the modules are innate and they have evolved

Question 35

Describe Gauthier and Tarr's processing requirements hypothesis for why there is functional organisation in the ventral stream and some examples of this hypothesis

Answer 35

 Processing requirements (Gauthier, Tarr) o FFA is not a face area, but related to expertise in discriminating members of perceptually homogenous class  Also activated by objects of expertise • E.g activation of FFA by birds in bird experts • Ventral occipitotemporal cortex is involved in object recognition, and the engagement of this region, including FFA, increases with expertise  FFA activation gets stronger across development o Organisational principle is process and modules are shaped by experience

Question 36

Describe the network requirements hypothesis for why there is functional organisation in the ventral stream and some examples of this hypothesis

Answer 36

 Network requirements o Certain brain areas may be specialised for certain types of information by virtue of other areas that they are connected to  FFA is a visual area that is strongly connected to areas important for emotional and social processing • Superior Temporal Sulcus (STS), amygdala  PPA is not a place area, but a spatial layout module • Strong connections with the posterior parietal lobe, retrosplenial cortex and hippocampus  WWFA becomes specialised for words • Strong connections with language areas

Question 37

Describe the anatomy of the dorsal stream

Answer 37

 Comes from the superior longitudinal fasciculus- takes a dorsal path from the striate cortex and other visual areas, terminating mostly in the posterior regions of the frontal lobe

Question 38

Describe the receptive fields and cellular representation in the dorsal stream, and how this contributes to its function?

Answer 38

 Representation in the dorsal stream • Neurons in the parietal lobe have large, nonselective receptive fields that include cells representing both the focal and periphery o Ideally suited for detecting the presence and location of a stimulus, especially one that has just entered the field of view

Question 39

Describe the anatomy of the ventral stream

Answer 39

 Inferior longitudinal fasciulus follows a ventral route from the occipital striate cortex into the temporal lobe

Question 40

Describe the receptive fields and cellular representation in the ventral stream, and how this contributes to its function?

Answer 40

 Representation in the ventral stream • Neurons in the temporal lobe have a large receptive fields that are much more selective and always represent foveal information o The disproportionate representation of central vision appears to be ideal for a system devoted to object recognition

Question 41

Describe the parts of the brain that process different aspects of facial properties

Answer 41

 Note: FFA is important for processing invariant facial properties, whereas the superior temporal sulcus is important for processing more dynamic features

Question 42

Describe the anatomical activation to inanimate objects

Answer 42

o Inanimate objects produce stronger activation in the medial regions of the ventral stream (the medial fusiform gyrus, lingual gyrus and parahippocampal cortex

Question 43

Describe the anatomical activation to animate objects

Answer 43

o Animate objects produce stronger activation in more lateral regions (the lateral fusiform gyrus and inferior temporal gyrus)

Question 44

What is object constancy?

Answer 44

o Object constancy- the ability to recognise an object in countless situations

Question 45

What are the 3 factors which influence and contribute to the principle of object constancy?

Answer 45

 Sensory information depends highly on viewing position • The human perceptual system is adept at separating changes caused by shifts in viewpoint from changes intrinsic to an object itself  Sensory information depends on its illumination  Sensory information depends on the object’s surroundings • A scene is often separated into its components

Question 46

Is recognition influenced by frame of reference?

Answer 46

• View-dependent vs view-invariant recognition o Recognition is dependent on the frame of reference o Recognition is independent of the frame of reference o Both dependent and independent frame of reference recognition may be used  Two hemispheres may process information in different ways

Question 47

Describe the theory that recognition is dependent on the frame of reference and a limitation to that theory

Answer 47

o Recognition is dependent on the frame of reference  Posits that people have a cornucopia of specific representations in memory- we simply need to match a stimulus to a stored representation  Ability to recognise that two stimuli are depicting the same object is assumed to arise at a later stage of processing  Limitation- • Places a heavy burden on perceptual memory as each object requires multiple representations in memory, with each associated with a different vantage point o Might be fixed if it is assumed that recognition processes are able to match the input to stored representations through an interpolation process

Question 48

Describe the theory that recognition is independent on the frame of reference and a limitation to that theory

Answer 48

o Recognition is independent of the frame of reference  Perceptual system extracts structural information about the components of an object and the relationship between these components  Key to successful recognition is that critical properties remain independent of viewpoint

Question 49

Describe the hierarchical theory of object perception

Answer 49

o Cells in the initial areas of the visual cortex code elementary features such as line orientation and colour o The outputs from these cells are combined to form detectors sensitive to higher order features such as corners or intersections o The process continues as each successive stage codes more complex combinations

Question 50

Describe the grandmother cell hypothesis for object recognition and its limitations

Answer 50

• Grandmother cell hypothesis- o Gnostic unit- the type of neuron that can recognise a complex object  Grandmother cell hypothesis – recognition arises from the activation of neurons that are finely tuned to specific stimuli  Limitations- • Cannot account for how it is possible to perceive novel objects • Does not account for how an object can change over time • Highly susceptible to error- if a single grandmother cell were to die, would lose all information pertinent to that cell

Question 51

Describe the ensemble activation hypothesis of object recognition and its advantages

Answer 51

• Ensemble activation hypothesis- o Recognition is not due to one unit but to the collective activation of many units  Account for why we can recognise similarities between objects and can confuse one visually similar object with another  Accounts for why we can recognise novel objects  If we lose one cell, not all information is lost

Question 52

What are the two types of processing in object perception? Define them and fit them to face, word and object processing

Answer 52

• Object perception o Two pathways of processing-  Analytic processing • A form of perceptual analysis that emphasizes the component parts of an object, a mode of processing that is important for reading  Holistic processing • Form of perceptual analysis that emphasizes the overall shape of an object, a mode of processing that is important for face perception  Examples- • Face- holistic perception (holistic processing) • Words- perception of individual components of the word (analytic processing) • Objects- both a holistic perception and perception of individual components

Question 53

By whom was fMR adaptation pioneered by and when?

Answer 53

o An imaging paradigm pioneered by Malach, Grill-Spector and colleagues around late 1990s

Question 54

What is the purpose of fMR adaptation and its advantages?

Answer 54

o Gain understanding of how neurons in a particular part of the brain probe for different properties of the object o Gets around some of the limitations in spatial resolution of fMRI  Allows us to discern if in a particular area there are neural populations with different response properties vs a homogeneous neuronal population  fMRI results in an average of thousands of neurons per voxel- spatial resolution is good but not great o A way of probing the nature of the object representations in a particular area  Are neurons invariant or variant with respect to size, location, orientation, etc.

Question 55

Describe how fMR adaptation can be used to study the process of neural adaptation and how neural adaptation can be used to determine the role of cells in response to stimuli

Answer 55

o BOLD response decreases when a stimulus is repeated  Approximates neural adaptation- repeated firing tires or sharpens neurons  If neurons are adapted, changing some aspect of the stimulus allows for recovery from the adaptation- this implies that a new population of neurons is responding to this new attribute • If there is no recovery from adaptation, this implies that the same adapted neural population responds irrespective of change in stimulus properties

Question 56

Describe Malach et al's experiment on determnining the role of lateral-occipital complex in object representation

Answer 56

o Applications- object representation in lateral-occipital complex (LOC)  Experiments- altered different aspect of stimulus (Malach et al.) • Changed size • Changed position in visual field • Adapt photographs of an object and tests with line drawings- change surface features • Shapes with motion cues

Question 57

What aspects of object representation does the activity of the lateral-occipital complex change with/nnot change with?

Answer 57

 LOC= high-level object shape representation  Results-activity invariant with respect to: • Size • Position in visual field • Image format (grayscale pic vs line drawing, shape defined by motion, luminance, stereo cues) • Visual or tactile input  But responses were more sensitive to viewpoint and illumination • Both can change shape of object very dramatically

Question 58

What are the two divisions of object representation in the lateral-occipital complex?

Answer 58

 Two divisions of object representation in LOC • LO (lateral division) • VOT (ventral division)

Question 59

What is the role of the lateral division of the lateral-occipital complex?

Answer 59

o More sensitive to changes in location and size than VOT o More sensitive to 2D shape features o A sub-region called LOtv (lateral occipital tactile visual area) is activated equally by visual and haptic input and is a multimodal shape area o LOtv codes the geometry of the shape/object and is multimodal

Question 60

Describe the results of Amedi et al.'s 2002 study on the lateral division of the lateral-occipital complex

Answer 60

 Amedi et al. (2002) | • Visual-tactile area LOtv activated by both seen and palpated objects, but not by characteristic sounds of object

Question 61

Describe the methods and results of Amedi et al.'s 2007 study on the lateral division of the lateral-occipital complex

Answer 61

 Amedi et al. (2007) • LOtv also activated by soundscapes of auditory shapes o Method:  Visual-to-auditory substitution device used for blind persons (the vOICe)  Person is trained to recognise visual images by soundscapes  This is not simply an association of an image with a sound, the idea is to learn to identify auditory shapes which can generalise  Visual image converted to soundscape by a visual-to-auditory sensory substitution algorithm (the vOICe)  Pixel location conveyed by sound frequency (up/down) and time (left/right)  Pixel brightness conveyed by loudness  Tested 2 blind and 5 sighted subjects trained to use vOICe to recognise objects  5 subjects with no vOICe training were taught to simply associate objects with soundscapes  After vOICe training, LOtv was activated by vOICe objects, compared to scrambled vOICe sounds or other object-specific sounds  LOtv was not activated by vOICe objects in the subjects with no vOICe training  LOtv is a multimodal shape area

Question 62

Describe the ventral division of the lateral occipital complex and its role/what it is activated/not activated by

Answer 62

• VOT (ventral division) o More invariant to changes in location and size than LOtv o Sensitive to perceived 3D shape (despite different 2D contours) o Not activated by haptic input o Correlates with recognition performance o Codes a more abstract identity representation and mediates awareness

Question 63

What are the four major concept to keep in mind when thinking about object recognition?

Answer 63

• When thinking about object recognition, there are four major concepts to keep in mind o Sensation, perception and recognition drefer to distinct phenomena o People perceive an object as a unified whole, not as an entity separated by its color, shape and details o Although our visual perspective changes, our ability to recognise objects remains robust o Memory and perception are tightly linked

Question 64

What is visual agnosia? Describe what they can and can't do

Answer 64

• Visual agnosia o Agnosia- not knowning/loss of knowledge  Failure of knowledge or recognition o Visual agnosia- a failure to make sense of visual information, to know what it represents  However, the person is not blind- elementary visual function is intact  Can recognise things from other modalities • Loss of object from vision only o Patients with visual agnosia are unable to recognise common objects presented to them visually. This deficit is modality specific. Patients can recognise an object when they touch, smell, taste or hear it

Question 65

What are the 4 major different types of visual agnosia?

Answer 65

 Apperceptive agnosias  Associative agnosias  Integrative agnosia  Category-specific deficits

Question 66

What is apperceptive agnosia, what can cause apperceptive agnosia and what are the symptoms of apperceptive agnosias (from a mild form to a severe form)

Answer 66

 Apperceptive agnosias- • Recognition deficits linked to problems in perceptual processing • The ability to achieve object constancy is compromised in patients with apperceptive agnosia • This type of disorder is more common in patients with right-hemisphere lesions, suggesting that this hemisphere is essential for the operations required to achieve object constancy • Are on different levels of severity o Very severe forms are caused by widespread bilateral damage to the occipital lobes (usually from CO poisoning as it prevents oxygen going to the brain- parts around lateral occipital area are not well irrigated in blood vessels: a decrease in oxygen amounts makes this part of the brain vulnerable )  Cannot discriminate even simple shapes  Cannot copy drawings  Cannot read  Cannot recognise faces that they know • Although if it is extremely severe, they will not recognise that they are looking at faces o Mild forms can recognise objects except in challenging conditions (from different views and lighting conditions)

Question 67

Describe case DF as a form of visual agnosia - What she suffered from/her brain abnormalities - Her symptoms - What she could/couldn't do - What information we got from studying her

Answer 67

case of visual form agnosia- Case DF (Milner et al. 1991) o 34 year old woman, suffered hypoxia from CO poisoning  Normal visual acuity  Could not discriminate small hue differences (but OK with primary colours)  Completely unable to identify objects, discriminate shapes, judge size or orientation  Could reach towards object correctly  Could shape and orient hand correctly to grasp objects  A striking dissociation between perception and vision for action • Perception-action dissociations in visual form agnosia o Explicit matching task shows that DF cannot recognize the orientation of a 3D object- however, when DF is asked to insert the card ( action task) her performance clearly indeicates that she had processedthe orientation of the slot  Had bilateral atrophy in LOC • DF also had some ventral activation in spared tissue when she was attempting to recognise objects, but it was more widespread than is normally seen in controls • In contrast, when asked to grab objects, DF showed robust activity in anterior regions of the inferior parietal lobe, similar to what is observed in neurologically healthy individuals

Question 68

What are associative agnosias? What can sufferers do/not do? What lesions is associative agnosias associated with?

Answer 68

• Patient can derive normal visual representations but cannot link them to information stored in memory o A normal percept stripped of its meaning • Failures of recognition that cannot be attributed to faulty perception o Patients can copy drawings, discriminate shapes, segment images but cannot identify objects o May be peripherally caused- due to disconnection between intact perceptual input and memory  Should be able to draw from memory o May be centrally caused- due to loss of stored object representations  Should not be able to draw from memory • Lesions causing associative agnosias tend to be in the occipital and temporal regions (vOT)-generally bilateral o Objects (and especially words) more associated with damage in the left hemisphere o Faces more in the right hemisphere (right fusiform gyrus)

Question 69

How are associative agnosias tested?

Answer 69

• Tested with the matching-by-function test- o Requires ability to group objects together by function, not percept similarity o Requires participants to understand the meaning of the object, regardless of its appearance

Question 70

What are category-specific deficits in object recognition?

Answer 70

 Category-specific deficits-Deficits of object recognition that are restricted to certain classes of objects

Question 71

What is visual object agnosia and what is it caused by?

Answer 71

• Visual object agnosia- inability to recognise objects | o Damage to LOC areas

Question 72

What is prosopagnosia and what is it caused by?

Answer 72

• Prosopagnosia- inability to recognise faces | o Damage to FFA

Question 73

What is alexia and what is it caused by?

Answer 73

• Alexia- inability to recognise words | o Damage to VWF

Question 74

What is topographical agnosia and what is it caused by?

Answer 74

• Topographical agnosia- inability to recognise familiar environments and landmarks o Damage to parahippocampal place area

Question 75

Are agnosias worse for inanimate objects than living ones? Why/why not?

Answer 75

• Note- Agnosias can be worse for living objects than inanimate ones o Manufactured objects are easier to recognise because they activate additional forms of representation o Although brain injury can produce a common processing deficit for all categories of stimuli, these extra representations may be sufficient to allow someone to recognise nonliving objects

Question 76

What is integrative agnosia?

Answer 76

 Integrative agnosia • Unable to integrate features into parts, or parts of an object into a coherent whole • Relies on recognizing salient features of parts instead of perceiving a whole object at a glance • Difficult to identify different overlapping objects

Question 77

What are simple dissociations and what can be concluded from them? What is one of their limitations?

Answer 77

o Simple dissociations  Patience can do A but not B  Could conclude that A and B tap into different (and independent) processes  But this could be due to a difference in task difficulty

Question 78

What are double dissociations and what can be concluded from them?

Answer 78

o Double dissociations  One patient can do A but not B  A different patient can do B but not A  Much more powerful evidence that A and B are independent

Question 79

What is the aim of cognitive neuroscience?

Answer 79

o Cognitive neuroscience aims to understand the relationship between mind and brain  Neural substrates of cognitive processes

Question 80

What is the aim of cognitive neuropsychology?

Answer 80

o Cognitive neuropsychology aims to understand the architecture of the normal cognitive system  Studying patients with brain damage is a convenient way of carving the system at its joints  Actual brain substrates are of no particular interest

Question 81

How can semantic memory be organised for object recognition?

Answer 81

• Semantic memory may be organised by category membership o Distinct representational systems for living and nonliving things, and perhaps further subdivisions within these two broad categories • Semantic memory may be organised based on object properties

Question 82

Describe Farah and McClelland's neural network model for object recognition and its consequences for living/non-living object recognition

Answer 82

• Neural network (Farah and McClelland) o Information is distributed across a number of processing units o One set of units corresponded to peripheral input systems, divided into a verbal and a visual system  Each of these is composed of 24 input units • Object representation involve a unique pattern of activation within these units o Second type of unit was semantic memory- visual and functional o When damage is restricted to visual semantic memory, the model had great difficulty associating the names and pictures correctly for living objects o When damage was restricted to functional semantic memory, failures were limited to non-living objects

Question 83

Who was HM and what happened to him?

Answer 83

• H.M. (Scoville and Milner 1957) o Suffered from severe epilepsy originating from his temporal lobe (hippocampus)-> underwent a bilateral removal of his medial temporal lobes to try to treat the epilepsy o Resulted in a memory disorder

Question 84

What was HM's memory deficit?

Answer 84

o H.M.’s memory deficit  Spared short-term memory (e.g. repeating a digit sequence)  Profound anterograde amnesia= inability to learn new information  Limited retrograde amnesia= inability to remember memories acquired prior to surgery • More distant past was spared • Selective memory loss for episodic memory as far back as a decade before the surgery, but only loss of semantic memory up to 2 years back  Memories for personally experienced events impaired  Semantic memory (e.g. facts, general knowledge) spared • Could also acquire some new semantic knowledge  Procedural (skill) memory spared • Mirror-drawing • Motor sequence learning  Priming (a form of implicit memory) spared

Question 85

What is anterograde amnesia?

Answer 85

• Anterograde amnesia- loss of memory or events that occur after a lesion or other physiological trauma

Question 86

What is retrograde amnesia?

Answer 86

• Retrograde amnesia- loss of memory for events and knowledge that occurred before a lesion or other physiological trauma

Question 87

What concepts were discovered from HM's injury?

Answer 87

 MTL (medial temporal lobe) is crucial for acquiring new long-term memories and plays a time-limited role in their storage or retrieval  Not all types of memories depend on the MTL

Question 88

What parts of HM did his surgery remove?

Answer 88

``` o HM’s surgical resection  Temporal pole  Amygdaloid complex • Sits at tip of temporal lobe  Entorhinal cortex • Wraps around hippocampus  Most of the hippocampal complex ```

Question 89

Who was the neuropsychologist who worked with HM

Answer 89

Milner

Question 90

What does the extent of amnesia depend on?

Answer 90

o Found that extent of the memory deficit depended on how much of the medial temporal lobe has been removed  The more posterior also the medial temporal lobe the resection had been made, the worse the amnesia was • Only bilateral resection of the hippocampus resulted in severe amnesia

Question 91

What are the 3 processing stages of learning and memory? Describe their definitions

Answer 91

``` • Encoding- o Process of incoming information and experiences, which creates memory traces o Two separate steps:  Acquisition • In sensory buffer  Consolidation • Changes in the brain stabilise a memory over time • Storage- o Retention of memory traces • Retrieval- o Accessing stored memory traces ```

Question 92

What are the components of memory?

Answer 92

``` • Short-term memory o Iconic memory o Working memory • Long-term memory o Declarative memory (explicit) o Non-declarative memory (implicit) ```

Question 93

Describe iconic memory in terms of timespan, capacity, awareness level and mechanism of memory loss

Answer 93

 Milliseconds to seconds  High capacity  No conscious awareness  Mainly lost through decay

Question 94

Describe working memory in terms of timespan, capacity, awareness level, mechanism of memory loss and purpose

Answer 94

 Seconds to minutes  Limited (7+-2 items)  Conscious awareness  Mainly lost through interference and decay  Represents a limited capacity store for retaining information over the short term (maintenance) and for performing mental operations on the contents of this store (manipulation)

Question 95

What are the two types of declarative long-term memory and briefly what are they for?

Answer 95

 Events (episodic memory) |  Facts (semantic memory)

Question 96

What is episodic memory

Answer 96

• Specific personal experiences from a particular time and place • Episodic memory contains contextual information about where and when some event (what) took place o Memories of events that the person has experienced that include what happened, where it happened, when, and with whom • Autonoetic consciousness o Self-referential memory

Question 97

What is semantic memory

Answer 97

• World knowledge, object knowledge, language, conceptual priming • Memory for semantic facts is generally free of experiential context o Includes personal semantics • Noetic consciousness o More about knowing • Objective knowledge that is factual in nature but does not include the context in which it was learned

Question 98

What is the anatomy of long-term declarative memory?

Answer 98

 Anatomy: MTL, middle diencephalon (including thalamus), neocortex

Question 99

Describe the timeframe, capacity, awareness level, mechanism of loss and the definition of long-term declarative memory

Answer 99

 Consists of our conscious memory for both facts we have learned (semantic memory) and events we have experienced (episodic memory)

Question 100

What are the four different types of non-declarative memory?

Answer 100

``` o Non-declarative memory (implicit)  Procedural memory  Perceptual representation  Classical conditioning  Non-associative learning ```

Question 101

Describe the time frame, capacity, level of awareness, mechanism of loss and definition of long-term non-declarative memory

Answer 101

```  Minutes to years  High capacity  No conscious awareness  Loss through interference  Non-conscious memory that cannot be verbally reported, often expressed through the performing of procedures (procedural memory) ```

Question 102

What is procedural memory and what is its anatomy?

Answer 102

 Procedural memory • Skills (motor and cognitive) • Anatomy: Basal ganglia, cerebellum

Question 103

What are the types perceptual representation and what is its anatomy?

Answer 103

```  Perceptual representation • Perceptual priming • Conceptual priming • Semantic priming • Anatomy- Perceptual and association cortex ```

Question 104

What is perceptual priming?

Answer 104

o Structure and form of objects and words can be primed by prior experience; depending on the stimulus, the effects persist for a few hours to months o Priming is modality specific

Question 105

What is conceptual priming?

Answer 105

o Doesn’t last as long as perceptual priming | o Affected by regions of the lateral temporal and prefrontal regions

Question 106

What is semantic priming?

Answer 106

``` o Prime and target are different words from the same semantic category o Brief (lasts only a few seconds) ```

Question 107

What is classical conditioning and its anatomy?

Answer 107

 Classical conditioning • Conditioned responses between two stimuli o A conditioned stimulus (CS, an otherwise neural stimulus to the organism) is paired with an unconditioned stimulus (US, one that elicits an established response from the organism) and becomes associated with it o The conditioned stimulus will then evoke a conditioned response (CR) similar to that typically evoked by the unconditioned stimulus (the unconditioned response, UR) • Anatomy- variety of sites including amygdala, cerebellum…

Question 108

What are the two types of non-associative learning and its anatomy?

Answer 108

 Non-associative learning • Habituation and sensitisation • Anatomy- variety of sites

Question 109

What is habituation?

Answer 109

o Habituation- the response to an unchanging stimulus decreases over time

Question 110

What is sensitization?

Answer 110

o Sensitization- response increases with repeated presentations of the stimulus

Question 111

Describe the location of the perirhinal cortex and parahippocampal cortex

Answer 111

• Perirhinal cortex and parahippocampal cortex are both on the parahippocampal gyrus (on top of hippocampus) o Perirhinal cortex- more anterior o Parahippocampal cortex- more posterior

Question 112

Describe the postulated roles of the hippocampus in memory

Answer 112

• Hippocampus o Has been proposed to play a permanent role in retrieving detailed contextual memory but is not necessary for retrieval once detail is lost and memory has generalized o The hippocampus is critical for the formation of long-term memory, and the cortex surrounding the hippocampus is critical for normal and hippocampal memory function o During retrieval, the hippocampus is selectively active only for objects that are actually correctly recollected instead of merely familiar, thus indicating an episodic memory o Relational memory theory proposes that the hippocampus supports memory for all manner of relations  However, it is also suggested that the specific relational information for items stored in long-term memory may be coded during retrieval by reactivation of the neocortical areas that provided input to the hippocampus during the original encoding

Question 113

Describe the anatomical process of memory formation

Answer 113

o Unimodal and polymodal association areas (frontal, temporal, and parietal lobes) Perirhinal cortex and parahippocampal cortex Entorhinal cortex -->Hippocampal complex (Dentate gyrus-> CA3-> CA1-> Subicular complex)  Entorhinal cortex also gives and receives input from other direct projects  The entorhinal cortex can directly project to all the components of the hippocampus separately  The entorhinal cortex can receive input from CA1 and the subicular complex  All inputs and outputs of the hippocampus go through the entorhinal cortex

Question 114

Describe the role of the perirhinal cortex in memory

Answer 114

o Familiarity-based item recognition o Learning associations about and between objects o Object perception  Especially important when object might share low-level features with other objects  Resolving featural ambiguity and identifying specific individuals defined by very particular configurations of features  What an object is o High level area of ventral stream

Question 115

Describe the evidence surrounding the role of the perirhinal cortex in memory

Answer 115

 Lesions lead to impairments in recognising objects, words, faces  fMRI- Activations in PRC during learning correlate with later ratings of familiarity • Davachi et al. (2003) o Made people learn from a variety of different tasks and later asked them if they remembered the item and the task it came from, just the items but not the task it came from, or didn’t remember the item o Perirhinal cortex fired when remembered item and context or item only, but not misses o Hippocampus only fired when remembered the item and context, but not when only the item was remembered or the item not remembered at all o High level area of ventral stream

Question 116

Where does the perirhinal cortex mostly project to?

Answer 116

o Projects mostly to anterior parts of the hippocampus

Question 117

Describe the role of the parahippocampal cortex

Answer 117

• Parahippocampal cortex (PHC) o Recollection of context information  Activations in PHC during learning and retrieval are high when context is successfully remembered o Both parahippocampal cortex and hippocampus are important for coding context  Similar activation pattern to the hippocampus during recollection tasks o Autobiographical memory  Activates more when recalling events that are personally important/participated in yourself o Spatial memory and navigation  Where an object is o Scene perception

Question 118

Describe the main connections of the parahippocampal cortex

Answer 118

o Projects mostly to posterior parts of the hippocampus o Has strong connections with retrosplenial cortex (which is also important for autobiographical memory and spatial memory/navigation)

Question 119

What is the binding of items and contexts model?

Answer 119

• Items (perirhinal cortex) and context (parahippocampal cortex) not bound until hippocampus- hypothesis that hippocampus binds items and contexts together o Binding of items and contexts model- the perirhinal cortex represents information about specific items (e.g. who and what), the parahippocampal cortex represents information about the context in which these items were encountered, and processing in the hippocampus binds the representations of items with their context

Question 120

What are the two main theories of memory consolidation and who is responsible for each?

Answer 120

* Standard consolidation theory- (1980s Squire et al.) | * Multiple trace theory (Nadel and Moscovitch 1997)

Question 121

Describe how memory is obtained and processed in the standard consolidation theory and then retrieved

Answer 121

• Information initially represented in different parts of neocortex is bound together into a memory trace by the MTL (and possibly the diencephalon) o Modality-specific representations in the neocortex e.g. visual aspects perceived by visual cortex o The neocortex is crucial for the storage of fully consolidated long-term memories, whereas the hippocampus plays only a temporary role • There is a short period of cohesion or synaptic consolidation lasting between seconds and minutes o Synaptic consolidation can include protein changes, synaptic changes… • This is followed by a prolonged period (years) of long-term (or system) consolidation • The MTL is initially necessary for reactivation of these memory traces, but the memory trace is eventually fully consolidated in the neocortex and becomes independent of the MTL • Same process for episodic and semantic memory

Question 122

Describe how memory is consolidated in the standard consolidation theory

Answer 122

• This is followed by a prolonged period (years) of long-term (or system) consolidation o Repeated activation of memory trace  Hippocampus may be important in this o Sleep  Replaying of memories during sleep  Slow wave hippocampal oscillations important for transferring information from hippocampus to cortex in conjunction with thalamus firing (fast spindles) • Sleep-related reply- where activity is replayed in the sanem temporal order as it was experienced o More tightly related to memory consolidation • Reverse-order awake replay of neural activity- may reflect a mechanism that permits recently experienced events to be compared to their memory trace and may potentially reinforce learning

Question 123

What is the temporal gradient in retrograde memory and what consolidation theory is it supported by?

Answer 123

• Standard consolidation theory- (1980s Squire et al.) • There is a temporal gradient in retrograde memory o Events and facts acquired more recently are more severely affected as they haven’t consolidated properly o More distant past memories better preserved o Retrograde amnesia tends to be greatest for the most recent events o Otherwise known as Ribot’s law

Question 124

What types of memory does the standard consolidation theory apply to?

Answer 124

• Applies equally to all types of declarative memory: o Episodic memory of personally experienced events o Semantic memory of facts about the world and public events o But not general semantics- i.e. conceptual knowledge, words

Question 125

What are challenges to the standard consolidation theory/limitations?

Answer 125

• Challenges to standard consolidation theory- o Some patients (including HM in retrospect) do not show a clear temporal gradient in retrograde memory  Retrograde amnesia can be very extensive (decades)  Even when old memories are retained, careful testing shows that they are more schematic and lacking in rich detail  Not the level of detail needed to re-experience the event o Dissociations in temporal gradients for different types of memory  Personally experienced episodic memories (autobiographical memory) often impaired for all of the patient’s past  Semantic memories more likely to show a temporal gradient, with better recall of older memories

Question 126

How are memories encoded and processed in the multiple trace theory?

Answer 126

• Multiple trace theory (Nadel and Moscovitch 1997) o Hippocampal complex (hippocampus and subiculum) automatically encodes all aspects of experience, represented at different neuronal sites  Neocortical sites-first process specific qualities of memory (e.g. visual information in visual cortex) o Hippocampal complex acts as an index or pointer to neurons that represent the information and binds the whole episode into a memory trace o Hippocampal complex provides the spatial context and keeps an index of where all different aspects of experience are represented o Re-activation of memory occurs in different neuronal and experiential context  The more times a memory is retrieved, the more traces are set down o Results in a new memory trace, because hippocampus automatically encodes all attended information  Traces share some or all of the information about the initial episode • Not every element may be activated and new elements may be re-incorporated

Question 127

How does memory consolidation and retrieval work in multiple trace theory?

Answer 127

o Multiple traces facilitate extraction of factual information common to all, which becomes independent of episodic context  Episodic content may be different across different reactivations  This is how a temporal gradient for semantic information (for facts) is formed o Older memories have more traces, so are more resistant to damage and have multiple retrieval routes

Question 128

Describe the different storage and retrieval of episodic vs semantic memories in the multiple trace theory

Answer 128

o However, episodic (spatial and temporal) context continues to be dependent on the hippocampal complex for as long as the memory trace is viable  No temporal gradient for autobiographical episodic memories  Long-term stores for semantic information rely solely on the neocortex while episodic memory, consolidated or not, continues to rely on the hippocampus for retrieval

Question 129

What evidence supports the multiple trace theory?

Answer 129

• Imaging studies supporting multiple trace theory o Ryan et al. 2001 found no difference in patterns of hippocampal activation for recall of recent (less than 4 years) and remote (more than 20 years) memories  Hippocampus is not sensitive to age of the memory o Gliboa et al. (2004) found that hippocampal activity was correlated with the vividness of re-experiencing the memory, rather than age of memory per se

Question 130

What are the two parts of the thalamus important in memory?

Answer 130

• Two parts of the thalamus important in memory- o Anterior thalamus o Dorsomedial nucleus of thalamus

Question 131

Describe the extended hippocampal diencephalic system

Answer 131

o Unimodal and polymodal association areas (frontal, temporal, and parietal lobes) Perirhinal cortex and parahippocampal cortex Entorhinal cortex -->Hippocampal complex (Dentate gyrus--> CA3--> CA1--> Subicular complex)-->Fornix--> Mamillary bodies--> Anterior thalamic nuclei--> prefrontal cortex and hippocampus  Entorhinal cortex also gives and receives input from other direct projects  The entorhinal cortex can directly project to all the components of the hippocampus separately  The entorhinal cortex can receive input from CA1 and the subicular complex  All inputs and outputs of the hippocampus go through the entorhinal cortex  Fornix also inputs to the prefrontal cortex  Prefrontal cortex also receives and inputs to the entorhinal cortex and the perirhinal cortex  Hippocampal complex projects to the anterior thalamus and the mammillary bodies via the fornix • Mamillary bodies also project to anterior thalamic nucleus via mammillothalamic tract  Anterior thalamus projects back to the hippocampus and amygdala mostly via the cingulum bundle (in cingulate gyrus)

Question 132

Describe the perirhinal-diencephalic system

Answer 132

o Unimodal and polymodal association areas (frontal, temporal, and parietal lobes) Perirhinal cortex Entorhinal cortex -->Medial dorsal thalamus --> Prefrontal cortex and perirhinal cortex  Perirhinal cortex can also project directly to prefrontal cortex and medial dorsal thalamus

Question 133

What is the proposed role of the hippocampal-diencephalic system?

Answer 133

• Aggleton and Brown (1999) proposed that the extended hippocampal-diencephalic system is involved in efficient encoding and, therefore, normal recollection of episodic memories o Damage to any part of this system produces similar memory impairments

Question 134

What is the proposed role of the perirhinal-diencephalic system?

Answer 134

• Perirhinal-diencephalic system is involved in familiarity based item recognition

Question 135

What are the symptoms of Korsakoff's syndrome and what is it caused by?

Answer 135

• Korsakoff’s syndrome (Korsakoff 1889) o Profound amnesia  Severe anterograde amnesia  Retrograde amnesia  Confabulation • Make something up when they don’t know the answer/include in recollections elements that are not true o Caused by damage to the diencephalon  Dorsomedial and anterior nuclei of the thalamus  Mamillary bodies  Also often additional atrophy of the prefrontal cortex o Due to thiamine (B1) deficiency in chronic alcoholism

Question 136

Describe the case of JG: - Issue - Demographic - Symptoms - Anatomy - Usefulness

Answer 136

• Case JG o Isolated retrograde amnesia in a patient with a thalamic lesion o 33-year-old man originally from the UK, immigrated to Australia 5 years ago o Episode of flu-like symptoms and somnolence, following which he could not remember anything about his own past  Profound retrograde amnesia o Intact anterograde memory day-to-day and on extensive testing o MRI: acute right thalamic lesion, as well as an older bilateral lesion, affecting parts of the medio-dorsal nucleus and mammillo-thalamic tract o Autobiographical memory and personal semantics severely impaired  Some patchy memory during the last 5 years  Reverse temporal gradient for his retrograde memory o Recollection and recognition were both impaired o 12 months later, he had some preserved autobiographical memory for events within the last 12 months, but still impaired for the more distant past o Informs us that thalamus is important in autobiographical memories

Question 137

Where is the retrosplenial cortex?

Answer 137

• Retrosplenial cortex comprises Brodmann areas 29 and 30 | o Behind the splenium

Question 138

What are the connections to and from the retrosplenial cortex?

Answer 138

• Strong anatomical connections with a range of memory structures o RSC receives input and gives input to the dorsolateral prefrontal cortex, the parietal and occipital cortex, the hippocampus and the anterior thalamic nucleus  Hippocampus and anterior thalamic nuclei receive input and give input to each other  Dorsolateral prefrontal cortex and parietal/occipital cortex receive input and give input to each other

Question 139

What occurs when there are lesions to the retrosplenial cortex (in rats and humans specifically)

Answer 139

• Lesions to RSC impair spatial memory and navigation in all species o In rats, also impairments in contextual fear conditioning (abolishes the fear conditioning), and active avoidance in a two-way shuttle box • In humans, lesions to RSC lead to severe impairments in episodic memory and spatial disorientation

Question 140

What is the role of the retrosplenial cortex

Answer 140

• RSCs are important for contextual memories that rely on spatial representations • RSC may play a translational role between allocentric and egocentric spatial reference frames o Orientation of self in space o Situating self in a recollected memory episode, seeing it from a particular viewpoint

Question 141

What is an allocentric reference frame?

Answer 141

o Allocentric reference frame- frame that is based on external environment  Layout of an environmental and how different landmarks/objects are positioned relative to each other in that environment

Question 142

What is an egocentric reference frame?

Answer 142

o Egocentric reference frame- frame based on the individual  From own point of view  Where things are in the environment relative to you

Question 143

What happens to the retrosplenial cortex in Alzheimer's disease?

Answer 143

• RSC is one of the areas that becomes atrophic/impaired very early in Alzheimer’s disease

Question 144

What is the core network of autobiographical memory

Answer 144

• Core network o Medial and lateral temporal lobes o Medial and ventro-lateral frontal lobes o Retrosplenial/posterior cingulate cortex o Temporo-parieto-occipital junction

Question 145

What brain areas are active in episodic future thinking? Are patients with amnesia able to episodic future thinK?

Answer 145

• Episodic future thinking o Areas in the core network also activate when subjects try to imagine future events o Patients with amnesia also have difficulty imagining future events

Question 146

What is memory and its use?

Answer 146

• Memory is a constructive process that allows recollection of the past and imagination of the future o More adaptative way of using past knowledge-> use of information to imagine what would happen in future circumstances/ how you should act

Question 147

What are the theories of the role of the core network of regions involved in episodic memory? Describe each

Answer 147

o Constructive episodic stimulation (Addis and Schacter)  Active constructive process of constructing past and future o Scene construction (Hasssabis and Maguire)  Thinking about memory episodes requires you to reconstruct scene in which episode took place-contextual aspect o Self-projection and mental time travel (Buckner and Caroll)  Allows to project yourself into context of past and future o Creating situational models (Ranganath and Ritchey)  Two systems in the brain that don’t tightly interact with each other: • Anterior temporal system • Posterior medial system (PM)

Question 148

In the creating situational model (Ranganath and Ritchey) for the role of the core network of regions involved in episodic memory, what is the role of the anterior temporal system and what does it anatomically contain? What is it vulnerable to?

Answer 148

o Item recognition and assessing the significance of entities o Social interaction and emotional processing  Noetic consciousness o Reward history associated with particular items, association of faces with names o Objects and people o Anatomically contains:  Anterior hippocampal formation  Perirhinal cortex  Lateral orbitofrontal cortex and amygdala  Ventral temporopolar cortex o Vulnerable to frontotemporal/semantic dementia

Question 149

In the creating situational model (Ranganath and Ritchey) for the role of the core network of regions involved in episodic memory, what is the role of the posterior medial system and what does it anatomically contain?

Answer 149

o Episodic/autobiographical memory and situational models  Autonoetic consciousness -self-referential aspect o How to act and behave in a particular situation (schemas) o Anatomically contains:  Retrosplenial cortex  Parahippocampal cortex  Posterior hippocampal formation  Anterior thalamus, mamillary bodies, pre-and parasubiculum  Posterior cingulate, precuneus, angular gyrus, ventromedial prefrontal cortex (default network) o Vulnerable to Alzheimer’s disease

Question 150

What is the default mode network and how does it overlap with the core network?

Answer 150

• A distributed network of regions that are more metabolically active when a person is at rest compared to when they are engaged in a task o Linked to introspection and recall of episodes at rest • High degree of overlap with the core network o Medial prefrontal cortex o Medial parietal cortex (posterior cingulate/precuneus/RSC) o Inferior parietal lobe (angular gyrus) o Medial and lateral temporal lobe

Question 151

What is semantic memory and what are errors that can result from a semantic deficit?

Answer 151

• Stored conceptual knowledge about the world, objects, word meanings, facts and people • Not connected to any particular time and place (that is to an episode) • Shared across individuals in a culture • Errors from semantic deficits o Mostly lean towards prototypical representations of objects

Question 152

How is semantic memory tested for?

Answer 152

``` • General knowledge • Picture naming • Word-picture matching • Drawing from memory • Describe/define a concept • Answer questions about things • Sort pictures according to category • Match items according to semantic associations o Taps into general knowledge and semantic associations ```

Question 153

What 4 types of pathology are semantic memory impairments?

Answer 153

• Associated with 4 types of pathology: o Semantic dementia (SD)- one of the syndromes caused by fronto-temporal lobar degeneration o Herpes simplex viral encephalitis (HSVE) o Stroke (left hemisphere) o Alzheimer’s disease

Question 154

What is semantic dementia derived from?

Answer 154

o Semantic dementia (SD)- one of the syndromes caused by fronto-temporal lobar degeneration

Question 155

What is herpes simplex viral encephalitis and what neuroanatomical changes can it cause?

Answer 155

 Herpes Simplex Viral Encephalitis • Viral infection (herpes simplex) that can affect the brain, particularly the temporal and frontal lobes, resulting in widespread necrosis o This may be because it comes from olfactory bulb o Differs in extent from patient to patient and can be bilateral or unilateral o HSVE is associated with bilateral ATL lesions

Question 156

What are the semantic deficits that herpes simplex viral encephalitis produce? Give an example

Answer 156

• HSVE patients sometimes have category-specific semantic deficits o Living things are often distorted o Non-living things are often more precise • Amnesia for earlier episodes in one’s life and profound difficulty in learning new information o When semantic memory is affected, the deficit is often mild relative to the profound semantic deficits observed in SD • Deficits can also sometimes be modality-specific o E.g. Patient TOB could not produce information about living things in response to their spoken names, but could in response to pictures. He could produce information about non-living objects to both spoken name and picture

Question 157

What are the most prominent impairments in semantic memory that can result from a stroke in the left hemisphere?

Answer 157

``` o Stroke (left hemisphere)  Most prominent impairment in these strokes is aphasia, but poor performance on non-verbal semantic tests as well as in verbal comprehension can result from left-hemisphere stroke ```

Question 158

What is Alzhimer's disease and what neuroanatomical changes does it produce?

Answer 158

o Alzheimer’s disease  Impairment of episodic (autobiographical) memory  Ability to learn new information is progressively abolished  Hypometabolism in the bilateral medial temporal lobes, the thalamus, the posterior cingulate gyrus and other parts of the limbic system

Question 159

What is semantic dementia, and what type of cognitive abilities are impaired in semantic dementia/how/why?

Answer 159

• Progressive, selective loss of semantic knowledge when tested in any modality • No category-specificity • Profound loss of word meanings: evident in comprehension and production (empty speech) • Inability to recognise objects (agnosia) • Anomia o Failure to name objects, concepts and people, whether in response to stimulus presentation or in spontaneous speech o Reflects degraded knowledge of an object or concept • Other cognitive abilities (e.g. episodic memory) and other aspects of language (syntax, phonology, pragmatics) seem to be much better preserved in activities of daily living (although other deficits become evident on testing) • Semantic deficit is profound and pervasive in all modalities and categories • Loss of specific knowledge-> more general knowledge about categories o Greater impairment on more precise basic-level classification o This is because subordinate (specific) level information activates the anterior temporal lobe, but not basic information or superordinate (broad) information

Question 160

What type of neuroanatomical damage is apparent in semantic dementia?

Answer 160

• Early on in the disease, damage is only in anterior part of temporal lobe o Characterised by severe degeneration of anterior and lateral temporal lobe, bilateral but often asymmetric (and left more than right) o Belongs to the fronto-temporal dementia spectrum

Question 161

What four principal factors is the degree of success or failure in any semantic test in SD patients determined?

Answer 161

• Degree of success or failure in any semantic test in SD patients is determined by four principal factors o The severity or stage of progression of the disease o The familiarity of the objects o The object’s typicality o The specificity of information required by the task

Question 162

What are the two main theories for organisation of semantic memory?

Answer 162

* Distributed-only view | * Distributed-plus-hub view

Question 163

What is the distributed-only view of semantic memory organisation/how does it work?

Answer 163

o Semantic representation of an object/concept is distributed across different nodes that may encode aspects of that object  Semantic memories are stored in areas involved in perception and action  Different attributes are distributed around this network o Tasks can determine which parts of the representation is accessed o Category and modality-specific impairments are caused by loss of part of the network for a concept, but not all the network

Question 164

What are limitations of the distributed-only view of semantic memory organisation?

Answer 164

o Limitations  Fails to explain how generalisation across different members of the category occurs, even with different members that could be quite different- how are extremely members of a category recognised as being in the same category with this model? • Fails to explain higher order generalisations  Fails to capture the type of semantic and neural impairment that occurs in semantic dementia • Would suggest that all brain is damaged  Fails to account for semantic memory/knowledge that is largely not perceptual and is more abstract

Question 165

Describe the concepts in the distributed-plus-hub view of semantic memory organisation

Answer 165

o All tasks requiring semantic memory are mediated by a representation that is independent of the task (that is, shared by all tasks)  Intermediate representations that arise in the hub can capture the deep structure of concepts and hence can promote generalization across items that are conceptually related, even if they do not happen to have similar shapes, colours, associated actions,…  These representations are amodal in that they can be generated from any individual receptive modality and can be used to generate behaviour in any individual expressive modality o There is a hub of neurons in the anterior temporal lobe- all different connections between the nodes that make up a semantic representation of the concept- go via the neuron hub o If hub is damaged, lose control of network which could result in profound semantic deficit that covers all modalities and categories  Agrees with semantic dementia model

Question 166

Describe the role/identity of the hub in the distributed-plus-hub view of semantic memory organisation

Answer 166

 Hub keeps connections and directs flow of traffic amongst other nodes of semantic network  Hub supports the interactive activation of representations in all modalities, for all semantic categories  Semantic generalisation requires a single amodal hub-the neuroanatomical site of this hub is the anterior temporal lobe  Suggests that the ATL regions encode the similarity relations among various concepts, so that semantically related items are coded with similar patterns across ATL neurons  People’s ability to receive information in one modality and express it in another, to generalise across conceptually similar entities that differ in almost every specific modality, and to differentiate between entities that resemble each other in many modalities seem to depend on the ATL

Question 167

What are the limitations of the distributed-plus-hub view of semantic memory organisation

Answer 167

o Limitations- |  May be oversimplified

Question 168

Who was the parallel distributed processing network developed by?

Answer 168

McClelland and Rogers 2003

Question 169

Describe the features of the parallel distributed processing network

Answer 169

o Inputs- various entities o Outputs-various properties/attributes related to the input entities o Logical nodes- in what manner inputs and outputs are connected o Hidden layers that direct flow of associations through the network  Have different weights to guide traffics through networks so that inputs are connected to the right outputs

Question 170

Describe the workings of the parallel distributed processing network

Answer 170

o As you learn about members in a category, a category emerges from overlap between all instances o Differentiation between categories occurs when there is little overlap between instances of activation

Question 171

Describe how confusion/memory errors can occur in the parallel distributed processing network

Answer 171

o Certain categories and semantic neighbourhoods can be much more dense than others  This allows for more confusion to arise, especially if there’s noise in system or loss of neurons in the hidden layers  May be more vulnerable to category-specific deficits o In sparser neighbourhoods where there are fewer members of that category and categories are more distinctive, there may be fewer instances of confusion o With degradation of the network, enough of the structure of strongly represented categories is still available, but specific details are lost  Can stimulate switching off neurons or introduce noise in system to see what occurs in the model which can produce misidentification/misrecognition/loss of information or confusion errors respectively

Question 172

Describe Ralph, Lowe and Rogers 2007's use of the PDP model and the method of the study/what hypotheses it tested

Answer 172

o Comparison of deficits in HSVE and semantic dementia o Lambon Ralph, Lowe and Rogers (2007) directly compared a group of 7 HSVE patients and a group of 8 Semantic Dementia patients on the same battery of tests in order to see how patients differ in types and patterns of errors they make  Matched for severity of semantic impairment based on a word-picture matching task o Gave patients naming task  Naming pictures at the basic taxonomic level • There is also superordinate (category) level or subordinate level (specific) naming but was not performed in this experiment o Used computational models to test hypotheses about how the pathology in these different disorders affect area in the anterior temporal lobe in order to give rise to different patterns of deficits  Used computational model similar to PDP model to stimulate activity in semantic network and see what happens when they make different lesions in the network • Verbal descriptors • Visual features • Semantics (heteromodal) o Hidden layer • Somatosensory • Praxis • Olfaction • Sounds  Lesioned the model in two different ways that mimic the neural changes in SD vs HSVE

Question 173

Describe Ralph, Lowe and Rogers 2007's use of the PDP model and the results of the study

Answer 173

 Semantic dementia had harder difficulty with the naming task than HSVE patients, but HSVE patients demonstrated a higher level of category specific deficiencies  HSVE patients make more semantic errors than semantic dementia patients whilst semantic dementia patients make more general errors than HSVE patients • For SD, damage was simulated by removing a proportion of connections in the network • For HSVE, damage was stimulated by introducing noise in the weights of the connections o This is because in this pathology, tissue is still there but connections are disrupted o Found that patients and models demonstrated similar trends  When representations are distorted (HSVE), items are easily confused if they have overlapping representations (e.g. living things) category-specific deficits  When representations are dimmed (SD), items are only recognised at a coarse level (most robust to damage) gradual loss of specificity • Attributes that are more common across a category are more robust to damage and are more likely retained for longer in semantic deficits

Question 174

What are the two main arteries in the brain

Answer 174

• Two main arteries o Internal carotid artery o Vertebral artery

Question 175

What is the internal carotid artery and how does it enter the brain?

Answer 175

 Big blood vessel on side of neck  Enters the brain close to tip of temporal lobe and branches out in different directions- mostly irrigates anterior part of the brain

Question 176

What does the internal carotid artery divide into?

Answer 176

 Splits into anterior cerebral artery and middle cerebral artery

Question 177

Where is the anterior cerebral artery and what brain region does it irrigate?

Answer 177

Irrigates medial part of the frontal lobe and parietal lobe | • Anterior cerebral artery- hugs the corpus callosum

Question 178

Where is the middle cerebral artery and what brain region does it irrigate?

Answer 178

Irrigates lateral surface of the frontal, parietal, temporal and some of the occipital lobe • Middle cerebral artery- sits inside Sylvian fissure o Specifically supplies blood to:  Temporal lobe  Anterolateral frontal lobe  Parietal lobe  Basal ganglia (caudate and globus pallidus)  Adjacent white matter o Perisylvian area is the vascular domain of the middle cerebral artery and contains a number of language-related areas

Question 179

What can occur if there is a stroke in the middle cerebral artery

Answer 179

o If there is a stroke in the middle cerebral artery, can end up with language impairments (this is likely as language is lateralised, as are strokes) or motor impairments

Question 180

What is the vertebral artery and how does it enter the brain?

Answer 180

 Comes along the spine and comes into brain at base of skull and irrigates mostly the posterior part of the brain  Goes along the brainstem and pons (basillar artery)

Question 181

What does the vertebral artery branch into?

Answer 181

 Branches into cerebellar artery |  Basillar artery splits into two posterior cerebral arteries (one for each hemisphere)-

Question 182

What does the basillar artery irrigate?

Answer 182

• Mostly irrigate medial occipital lobes and medial/inferior temporal lobes

Question 183

What occurs if there is a stroke in the posterior cerebral artery?

Answer 183

• If there is a stroke in the posterior cerebral artery, could get visual impairments, agnosias, memory impairments o Strokes in this circulation system are less likely and effects of such a stroke would not be as catastrophic, as strokes are usually not bilateral

Question 184

How do the internal carotid and vertebral artery communicate?

Answer 184

• Internal carotid and vertebral artery communicate with each other through the posterior communicating arteries (provides connections between anterior and posterior circulation systems)

Question 185

What is an ischemic stroke and what are the chances of recovery?

Answer 185

o Ischemic stroke  Blockage in blood vessel (blood clot or dislodged fatty tissue)-> blockage can derive neurons of nutrients and neurons may die • Bad prognosis- little chance of recovery

Question 186

What is a hemorraghic stroke and what are the chances of recovery?

Answer 186

o Hemorraghic stroke  Ruptured blood vessel-> causes irritation, inflammation which can cause damage • There is a chance of recovery (neurons not necessarily dead)

Question 187

What are the speech areas in the brain?

Answer 187

• Speech areas- o The first is a motor area and contains representations of movement; the second is sensory, containing memory images of past sense impressions. The parietal lobe proper, which lies between them, is a transitional area

Question 188

Who was Pierre Paul Broca and what did he report/discover? Describe the patient (ability and neuroanatomical change)

Answer 188

• Pierre Paul Broca (1824-1880) o French surgeon, pathologist o Reported the case of Leborgne (Also known as Tan) in 1861  Had lost all ability to speak, could only say the syllable ‘tan’  At autopsy it was found he had a stroke in the inferior part of the frontal lobe in the left hemisphere o Concluded that this area (now called Broca’s area) was the speech centre

Question 189

Where is Broca's area located?

Answer 189

o Broca’s area located in the inferior frontal gyrus of the left hemisphere  Includes the pars triangularis and pars opercularis (or operculum)  Brodmann areas (BA) 44/45

Question 190

How did Brodmann's map come about?

Answer 190

• Brodmann- German pathologist that mapped areas of the brain that had different cytoarchitecture, and hence may have different structure o Came up with 52 areas

Question 191

Who was Carl Wernicke report and who was he?

Answer 191

o In 1894 reported two people with intact hearing but selectively impaired speech comprehension o Speech fluent but with nonsensical and distorted words o Proposed two brain areas involved in language

Question 192

Where is Wernicke's area?

Answer 192

o Located in the posterior third of the superior temporal gyrus  Brodmann area (BA) 41/42 and 22

Question 193

What tract are Wernicke's area and Broca's area linked by?

Answer 193

• Wernicke’s area and Broca’s area are linked by the arcuate fasciculus

Question 194

What are the major symptoms of Wernicke's aphasia?

Answer 194

• Characteristics of Wernicke’s aphasia o Severe anomia  Naming difficulties o Fluent and grammatical speech- but largely meaningless  Paraphasias (phonological approximations)  Jargon (completely novel non-words)  But motor aspect of speech is intact but content is largely meaningless o Impaired reading o Impaired comprehension o Impaired repetition o Thoughts are not in a logical sequence: start at the end of a thought and works back to the beginning o Loss of auditory representation of words o They have difficulty monitoring what they are saying: often don’t realise that they are saying the wrong thing

Question 195

What is the classical model of aphasia (possible aphasias), how they occur and what they produce? Who proposed this?

Answer 195

``` o Lichtheim (1885) and later revived by Geshwind in the 1960s.  Possible aphasias • Damage to Broca’s area o Broca’s (expressive) aphasia o Impaired production • Damage to Wernicke’s area o Wernicke’s (receptive) aphasia o Impaired comprehension • Damage to concept/semantic areas o Semantic impairments, agnosias, etc. • Damage to arcuate fasciculus o Conduction aphasia o Impaired repetition/reproduction of speech  Especially for meaningless words ```

Question 196

How are the speech areas in the brain connected/what are they and what are their roles?

Answer 196

 Connected areas for speech are: • Motor language area (Broca’s) o Implements speech planning and programming • Sensory language area (Wernicke’s) o Stores info about the word sounds (phonological lexicon) • Concepts (semantics) stored in other areas

Question 197

What is the clinical classification of expressive aphasia?

Answer 197

 Broca’s aphasia- expressive aphasia

Question 198

What is the clinical classification of Wernicke's aphasia?

Answer 198

 Wernicke’s aphasia- receptive aphasia

Question 199

What is the clinical classification of conduction aphasia?

Answer 199

 Conduction aphasia- disorder of repetition

Question 200

What is the clinical classification of transcortical aphasia?

Answer 200

 Transcortical aphasia-can repeat words they don’t comprehend

Question 201

What is the clinical classification of global aphasia?

Answer 201

 Global aphasia- lost all language (expressive and receptive)

Question 202

What are the uses/limitations of clinical classification aphasias?

Answer 202

o Useful for clinical management and localisation of damage | o Not so useful for understanding the neural basis of language processing

Question 203

What are the symptoms of conductive aphasia? What causes conductive aphasia

Answer 203

o Impaired repetition, with relatively good spontaneous speech and comprehension  Usually worse for non-words • For meaningful words, could go around through the semantic system and then repeat it instead of going straight through the arcuate fasciculus o Phonemic paraphasias in spontaneous speech, which get progressively closer to target word o Thought to be caused by damage to the arcuate fasciculus (fibre bundle connecting Wernicke’s and Broca’s areas)  Disconnection between areas involved in word recognition and word production

Question 204

What are the major symptoms of Broca's aphasia?

Answer 204

• Non-fluent • Difficulties articulating o Apraxia of speech (problems programming articulations) o Dysarthria (loss of control over articulations- that is slurred speech) • Anomia- word finding difficulties • Better comprehension- but not perfect • Absence of function words (the, a, on, etc)-that is telegraphic speech • Agrammatism- that is difficulty with complex grammatical structures o Both in production and in comprehension o Have particular trouble with passive voice • Often accompanied by other neurological signs: o Right sided weakness or hemiparesis (hand area is close to Broca’s area, so likely to be affected by the same stroke)  Reflexes much brisker on right side- less control of muscle in that arm o Oro-facial apraxia (difficulties making skilled movements with the mouth

Question 205

What is an apraxia of speech?

Answer 205

• Apraxia of speech- disordered articulation

Question 206

Describe the samples of Dronkers (1996) study on apraxia of speech

Answer 206

``` o Dronkers (1996) studied 25 patients with apraxia of speech and 19 patients without apraxia of speed  All patients had lesions to left hemisphere ```

Question 207

What is the lesion overlay method?

Answer 207

o Used lesion overlay method  For each patient, traced around the lesion and superimposed all traces onto a brain template-> can then see the areas of overlap in lesions in patients

Question 208

Describe the method and results of Dronkers (1996) study and why the evidence was so strong

Answer 208

o Used lesion overlay method o ALL patients with apraxia of speech had a common area of damage- precentral gyrus of the insula  Systematic analysis of both patients who do and don’t have the deficit allows for focusing of area critical for particular function o NONE of the patients without apraxia of speech had a lesion there o Apraxia of speech does not appear to be caused by damage to Broca’s area proper

Question 209

What is voxel-based lesion symptom mapping and what kind of information does it give?

Answer 209

* A technique for determining regions that are responsible for specific functional impairment * Gives causal information (unlike fMRI information)

Question 210

Describe the process of voxel-based lesion symptom mapping

Answer 210

o Includes both patients with a particular symptom and those without o Take brain scans from everybody then create a brain template o Divide brain template into voxels (3D pixel) o For each brain voxel (e.g. 0.5 mm brain area) divide patients into two groups- lesion present or lesion absent in that area o At each voxel, perform t-test on dependent measure of language e.g. score on language test o Produces a map of areas significantly correlated with the language measure- a bit like an fMRI map o Colder colours- low significance o Warmer colours- high significance

Question 211

Which regions are involved in language comprehension?

Answer 211

 Middle temporal gyrus (posterior BA 21 and superior BA 37 + surrounding white matter)  Anterior superior temporal gyrus BA 22  Superior temporal sulcus and angular gyrus (parietal lobe, BA 39)  Inferior frontal areas around Broca’s area (BA 45/BA 47 and BA9/BA46)

Question 212

Which region is involved in single word comprehension and naming?

Answer 212

 Middle temporal gyrus (posterior BA 21 and superior BA 37 + surrounding white matter)

Question 213

Which region is involved in comprehension of simple sentences?

Answer 213

 Anterior superior temporal gyrus BA 22

Question 214

Which region is involved in comprehension of working memory for complex syntax?

Answer 214

 Inferior frontal areas around Broca’s area (BA 45/BA 47 and BA9/BA46)= working memory for complex syntax

Question 215

Did Broca's area and Wernicke's area correlate with comprehension deficits?

Answer 215

 But Broca’s area and Wernicke’s area did not correlate with comprehension deficits

Question 216

What are the 3 main cortical language circuits and who were they proposed by?

Answer 216

• Cortical language circuit (Friederici 2012) o During auditory sentence comprehension (semantic route)- ventral route o During auditory sentence comprehension (syntactical comprehension route)- dorsal route o Auditory-to-motor mapping

Question 217

Describe the ventral route of auditory sentence comprehension, its purpose, and its development

Answer 217

o During auditory sentence comprehension (semantic route)- ventral route:  Auditory information first into primary auditory cortex-> anterior superior temporal gyrus-> inferior frontal cortex (BA 45/47) via ventral connections  Back projections from frontal cortex to superior temporal gyrus and middle temporal gyrus via ventral route support top-down semantic processes  Route develops quite early (3-5 years of age)

Question 218

Describe the dorsal route of auditory sentence comprehension, its purpose, and its development

Answer 218

o During auditory sentence comprehension (syntactical comprehension route)- dorsal route:  Primary auditory cortex-> anterior superior temporal gyrus-> frontal cortex (BA 44) via ventral connections  Back projections from frontal cortex to superior temporal gyrus/superior temporal sulcus via dorsal route (via arcuate fasciculus) support assignment of syntactical relations  Develops late (fully mature by 11 years old)

Question 219

Describe the auditory-to-motor mapping route of auditory sentence comprehension, its purpose, and its development

Answer 219

o Auditory-to-motor mapping  Primary auditory cortex-> posterior superior temporal gyrus-> premotor cortex via dorsal connections support auditory-to-motor mapping • Support babbling in babies • Operates in a bottom-up manner and already present at birth • Might subserve repetition

Question 220

Contrast the role of the ventral to the dorsal cortical language circuit

Answer 220

o Ventral circuit appears to be more important for semantic aspect of sentence processing whilst the more dorsal one appears to be more important for syntax/grammar aspect of sentence processing

Question 221

What are the limitations of Lichtheim's (1885) model of aphasia? What are the reasons for this limitation ad what can be done to overcome it?

Answer 221

• Limitations o Lesion-deficit correspondence does not always hold  E.g. not all patients with lesions to Broca’s area present with symptoms of Broca’s aphasia  Not all patients with classical symptoms of Broca’s aphasia have lesions in Broca’s area  Same holds for other types of aphasia  Reason: • Classical aphasias are syndromes associated with damage to particular vascular territories o Syndrome= a constellation of symptoms o A stroke affects a certain part of the brain (which may be large) , which may contain a number of different areas, each specialised for different functions • So damage to a brain area might often co-occur with a particular symptom, without playing a causal role in that symptom o To tease apart which brain area is responsible for which symptom, need to look at collection of syndromes, look at common symptoms and look at converging brain areas

Question 222

What is primary progressive aphasia and when does it mostly occur?

Answer 222

• Primary progressive aphasia is a focal neurodegenerative disorder presenting as an isolated and progressive language impairment o Other cognitive domains are well-preserved • Occurs mostly in the context of fronto-temporal lobar degeneration

Question 223

What are the three types of primary progressive aphasia?

Answer 223

o Non-fluent/agrammatic variant o Semantic dementia o Logopenic variant

Question 224

What are the main symptoms of non-fluent/agrammatic primary progressive aphasia and what neuroanatomical regions is it most associated with?

Answer 224

o Non-fluent/agrammatic variant  Main symptoms: • Agrammatism in language production and/or • Effortful, halting speech (apraxia of speech)  Additional features (2 of 3) • Impaired comprehension of grammatically complex structures • Spared single-word comprehension • Spared object knowledge  Associated with predominant left posterior frontal and insula abnormalities on imaging

Question 225

What are the main symptoms of semantic dementia primary progressive aphasia?

Answer 225

 Main symptoms • Impaired confrontation naming (pictures) and • Impaired single word comprehension  Additional features (3 of 4): • Impaired object knowledge • Surface dyslexia (inability to read irregular words) o Irregular words can only be read via the meaning • Spared repetition • Spared speech production

Question 226

What are the main symptoms of logopenic primary progressive aphasia and what neuroanatomical regions is it most associated with?

Answer 226

o Logopenic variant  Main symptoms • Impaired single-word retrieval in spontaneous speed and • Impaired repetition of sentences and phrases  Additional features (3 of 4) • Impaired object knowledge • Surface dyslexia (inability to read irregular words) • Spared repetition of single words • Spared speech production  Associated with predominant left posterior perisylbian or parietal abnormalities on imaging (in vicinity of Wernickes)

Question 227

In what disease does non-fluent and semantic dementia mostly occur?

Answer 227

• Interestingly, non-fluent and semantic dementia almost always occur in context of Pick’s disease

Question 228

In what disease does logopenic aphasia mostly occur?

Answer 228

• Logopenic variant almost always occurs in context of Alzheimer’s disease

Question 229

What is dementia? Describe

Answer 229

• Dementia- describes cognitive impairments that occur in the context of neurodegeneration o Decline of memory and(or) other cognitive abilities from a previous level of function, which must be sufficiently severe to cause impairment in occupational or social functioning  Change from a previous level of functioning, usually progressive  Multiple cognitive/behavioural domains affected  Impacts on the person’s activities of daily living

Question 230

Which cognitive deficits can appear in dementia and what is the brain area responsible for them? Describe which aspects of these cognitive categories can be deficient in dementia.

Answer 230

``` • Memory (medial temporal lobe) o Type: episodic, semantic, procedural o Process: encoding, recall, recognition of previously encountered information • Language (perisylvian fissure) o Comprehension and expression o Knowledge of grammatical rules o Naming objects and concepts o Reading and spelling • Visuo-perceptual skills (occipital posteriotemporal lobes) o Recognition of objects and faces o Spatial orientation o Construction, drawing • Praxis (parietal lobe) o Planning and executing skilled actions o Tool use o Dressing • Attention o Filtering relevant from irrelevant information o Manipulating information held in memory o Speed of processing o Sustaining mental effort o Spatial attention • Executive functions (tend to rely on frontal lobe of brain) o Organising information and behaviour o Planning o Mental flexibility o Abstract thought o Impulse control and drive/initiation ```

Question 231

Give examples of neurodegenerative diseases associated with dementia

Answer 231

``` o Alzheimer’s disease (70% of all dementias) o Fronto-temporal lobar degeneration o Vascular (multi-infarct) dementia (17% of all dementias) o Parkinson’s disease o Lewy body disease o Huntington’s disease o Cortico-basal degeneration o Progressive supranuclear palsy o HIV dementia ```

Question 232

What is the frequency of 40-65 year olds that have Alzheimer's disease?

Answer 232

o 1/1000 of 40-65 year olds

Question 233

What is the frequency of 65-70 year olds that have Alzheimer's disease?

Answer 233

o 1/50 of 65-70 year olds

Question 234

What is the frequency of 70-80 year olds that have Alzheimer's disease?

Answer 234

o 1/20 of 70-80 year olds

Question 235

What is the frequency of over 80 year olds that have Alzheimer's disease?

Answer 235

o 1/5 of over 80 year olds

Question 236

What is the best predictor of Alzheimer's disease?

Answer 236

• A disease of old age- best predictor of Alzheimer’s disease is age

Question 237

Why is normal aging a confounder of early Alzheimer's disease diagnosis?

Answer 237

• Normal aging can significantly affect the severity and pattern of neuropsychological deficits associated with early AD and reduce the saliency of the deficit profile as a diagnostic marker of the disease

Question 238

What could improve the ability to detect Alzheimer's disease in its earliest, preclinical stages?

Answer 238

• Consideration of both cognitive asymmetry and subtle declines in memory may improve the ability to detect AD in its earliest, preclinical stages

Question 239

What is Alzheimer's disease?

Answer 239

• Alzheimer’s disease- an age-related degenerative brain disorder characterized by neuronal atrophy, synapse loss, and the abnormal accumulation of amyloidogenic plaques and neurofibrillary tangles in medial temporal lobe limbic structures and association cortices of the frontal, temporal and parietal lobes

Question 240

What is the timeline of Alzheimer's disease progression and what does it depend on?

Answer 240

• Disease progression- approximately 8-10 years from first symptoms to death o Certain subtypes may progress more rapidly  Subtypes associated with genetics o Usually earlier onset tends to have more rapid progression

Question 241

By whom was Alzheimer's first described?

Answer 241

• First described by Alois Alzheimer in 1906 and by Kraepelin in 1920, who identified the beta-amyloid plaques and neurofibrillary tangles o Pathologically-defined entity

Question 242

What are the pathological symptoms of Alzheimer's and what are the impacts of this?

Answer 242

• Neurofibrillary tangles have been shown to have a strong predilection for cortical layers and cell types that support connections between functionally related cortical association areas o Cortical disconnection appears to lead to marked abnormalities in the interregional pattern of blood-flow activation elicited during the performance of cognitive tasks o Cortical dysconnectivity is a big problem in AD

Question 243

Who published the first clinical diagnostic criteria for Alzheimer's?

Answer 243

• McKahnn et al. 1984- published the clinical diagnostic criteria devised by the NINCDS-ADRDA Work Group on Alzheimer’s disease

Question 244

What is DSM-IV's diagnostic criteria for Alzheimer's disease?

Answer 244

o DSM-IV  Criterion A- multiple cognitive deficits, including: • Memory • One or more disturbances in language, praxis, visuo-spatial, executive functioning  Criterion B- the cognitive deficits each cause significant impairment in social or occupational functioning and represent a decline from previous levels of functioning  Criterion C- there is gradual onset and continuing cognitive decline  Exclusionary criteria- the cognitive deficits are not due to acute delirium, other systemic illnesses or substance abuse, or are better accounted for by a mood disorder

Question 245

What is DSM-V's diagnostic criteria for Alzheimer's disease?

Answer 245

o DSM-V  Re-terms dementia as major neurocognitive disorder • Allows for milder versions of cognitive disorder  Essentially the same as DSM-V, except a diagnosis does not require a memory impairment, as long as there is evidence of a genetic mutation known to cause Alzheimer’s disease  Acknowledges progress in our understanding of the biological bases of the disease and of the existence of atypical variants  These criteria are likely to keep evolving

Question 246

What are the essential factors to look at when diagnosing dementia?

Answer 246

o Diagnosing dementia-essentials  Clinical history of decline in cognitive function and impairment of daily living • Want to get this information from patient and someone who can verify it (like family member)  Objective evidence of cognitive and/or behavioural impairment on neuropsychological testing  Deficits and presentation can’t be explained by other conditions (e.g. stroke, brain tumour, mood disorder) • See if mood disorder treatment alleviates cognitive impairments  Preferably evidence of progressive decline across repeated neuropsych testing  Associated biomarkers- e.g. abnormalities on brain scans, abnormal cerebro-spinal fluid biomarkers, pathology findings on brain biopsy, genetic testing

Question 247

At what age is Alzheimer's disease typically presented?

Answer 247

o Presentation is after age 60

Question 248

What symptoms are typically present first in Alzheimer's disease and how is this identified?

Answer 248

o Memory impairment often the first presenting complaint and the most prominent  On testing, there is both a failure to encode information and to store this information in a more permanent way (that is, delayed recall is very poor and cueing doesn’t help retrieval) • Suggests AD results in a true loss of semantic knowledge rather than only an impaired ability to retrieve information from intact semantic memory stores

Question 249

What are ways of differentiating between mildly demented AD patients and normal older adults?

Answer 249

 Patients with early AD are particularly impaired on measures of delayed recall  To-be-remembered information is not accessible after a delay even if retrieval demands are reduced by the use of recognition testing  AD patients exhibit an abnormal serial position effect characterised by an attenuation of the primary effect, suggesting that they cannot effectively transfer information from primary memory to secondary memory  Semantic encoding is less effective in improving the episodic memory performance of patients with AD  Patients with AD have an enhanced tendency to produce intrusion errors on both verbal and nonverbal memory tests, presumable due to increased sensitivity to interference and/or decreased inhibitory processes

Question 250

What symptoms emerge as typical Alzheimer's disease advances

Answer 250

o As disease advances, language, visuo-spatial, executive functions become compromised  Ability to perform concurrent manipulation of information appears to be particularly vulnerable  Attention deficits are usually visible on dual-processing tasks and working memory tasks

Question 251

What symptoms is a typical presentation of Alzheimer's disease characterised by?

Answer 251

o Characterised by prominent amnesia (especially of episodic memory) with additional deficits in language and semantic knowledge, abstract reasoning, executive functions, attention and visuospatial abilities o General demeanour and personality usually preserved until late in the disease

Question 252

What is the pathology of typical Alzheimer's disease presentation?

Answer 252

o Distribution of neurofibrillary tangles and amyloid plaques  Posterior areas (parieto-occipito lobes), temporal lobes, dorsolateral prefrontal cortex, retrosplenial cortex, medial aspect of frontal lobe  Most severe atrophy or hypometabolism is in the mesial temporal lobe (including hippocampus), parietal lobes and dorsolateral prefrontal cortex  Atrophy in alzheimer’s disease- enlarged ventricles and sulci, atrophic hippocampus o Earliest changes occur in medial temporal lobe structures critical for episodic memory

Question 253

At what age is Alzheimer's disease atypically presented?

Answer 253

o Often earlier onset, 50s or even 40s

Question 254

What is the difference between typical and atypical Alzheimer's disease based on initial symptoms?

Answer 254

o Memory usually not compromised in early stages

Question 255

Describe the symptoms and pathology of visual variant Alzheimer's disease

Answer 255

o Visual variant AD or Posterior cortical atrophy  Visuo-spatial impairments (e.g. judging spatial location and relations, left-right orientation)  Visual agnosia (impaired object recognition, especially from less familiar viewpoints)  Apraxia (difficulties with complex actions, assembling things, dressing)  Significant brain changes in parietal and occipital lobes, relatively normal temporal and frontal lobes

Question 256

Describe the symptoms and pathology of frontal variant Alzheimer's disease

Answer 256

o Frontal variant alzheimer’s disease  Executive dysfunction (poor planning and organissation, impaired mental flexibility, concrete thinking)  Personality change  Significant brain changes in frontal lobes

Question 257

Describe the symptoms of lgopenic aphasia

Answer 257

o Logopenic aphasia  Start in language areas  First presenting symptom would be impairment in language that then spreads to other cognitive functions

Question 258

What are the three types of alzheimer's disease atypical variants?

Answer 258

o Visual variant AD or Posterior cortical atrophy o Frontal variant alzheimer’s disease o Logopenic aphasia

Question 259

By whom was fronto-temporal dementia first discovered? What are the pathological characteristics of this type of dementia?

Answer 259

• First described by Arnold Pick in 1892 and called Pick’s disease for a long time o Disease concentrated in frontal and temporal lobes (anterior and lateral) o Different pathology: Pick bodies

Question 260

What is the frequency of fronto-temporal lobar degeneration? How many cases of dementia does it account for?

Answer 260

• Second most common cortical dementia, although still fairly rare o About 2-10 in 10,000 • FTD accounts for 6-12% of all cases of dementia

Question 261

At what age is the onset of fronto-temporal lobar degeneration?

Answer 261

• Earlier onset- 40s to 50s

Question 262

What led to the Lund-Manchester criteria for FTD?

Answer 262

• Large clinico-pathological samples studied in Manchester (neary and Snowden’s group) and in Lund (Brun’s group) in the 1980s and 1990s o Lund-Manchester criteria for FTD

Question 263

What are the three main variants of fronto-temporal lobar degeneration?

Answer 263

o Behavioural variant o Sementic dementia o Progressive non-fluent aphasia

Question 264

Describe the behavioural variant of fronto-temporal lobar degeneration in terms of pathology and symptoms

Answer 264

```  Frontal lobe atrophy  Personality and behaviour change • Disinhibition, perseveration • Apathy • Emotional blunting • Over-eating, hyperorality  Executive dysfunction on neuropsych testing • Mental inflexibility • Concrete thinking • Planning problems  Memory and visuo-perceptual skills relatively spared ```

Question 265

Describe the semantic variant of fronto-temporal lobar degeneration in terms of pathology and symptoms

Answer 265

``` o Sementic dementia  Anterior-lateral temporal lobe atrophy (more common left)  Progressive loss of semantic knowledge  Visuo-perceptual skills preserved  Memory (relatively well) preserved  Personality preserved ```

Question 266

Describe the progressive non-fluent aphasia variant of fronto-temporal lobar degeneration in terms of pathology and symptoms

Answer 266

``` o Progressive non-fluent aphasia  Inferior frontal atrophy (around Broca’s area)  Non-fluent speech  Agrammatic language disorder  Visuo-perceptual skills preserved  Memory (relatively well) preserved  Personality preserved ```

Question 267

Describe the frequency of vascular dementia and the typical age of onset of this dementia

Answer 267

• Second most common cause of dementia after Alzheimer’s disease (about 2/3 non-Alzheimer cases) o Range- 0.3% in 65-70 year olds, 16% in over 80s o Can occur alongside Alzheimer’s dementia

Question 268

What is vascular dementia caused by?

Answer 268

* Caused by hypertension leading to multiple strokes in the brain * Onset of symptoms usually related to cerebro-vascular events

Question 269

Describe the progression pattern of vascular dementia

Answer 269

• Progression more step-wise with periods of plateau

Question 270

What are the cognitive deficits resulting from vascular dementia caused by subcortical ischemic vascular dementia?

Answer 270

• Distribution of lesions varies widely and so could the neuropsychological picture o Many small vessel infarctions in the white matter  A more subcortical neuropsychological picture • Slow speed of processing • Attention problems • Memory problems can be secondary to: o Attention difficulties o Difficulties initiating memory search • Motor and other neurological problems can be present o Weakness or paralysis

Question 271

What are the three main categories of vascular dementia?

Answer 271

• Largely three categories: o Multi-infarct dementia associated with multiple large cortical infarctions o Dementia due to strategically placed infarction o Subcortical ischemic vascular dementia due to subcortical small vessel disease

Question 272

What are the symptoms of dementia in Parkinson's disease and how common are they?

Answer 272

• Apathy, difficulty in getting going • Slowed mental processing • Attention impairments, especially shifting attention • Visuo-spatial impairments • Visual hallucinations • Memory-problems with recall • Cognitive impairments occur after motor disorder o Occur quite late • Relatively rare for generalised cognitive impairments