104 terms



Terms in this set (...)

Functional Motor System
Parallel hierarchical
Sensory feedback is crucially important in modulating the output of the motor system
Sensorimotor Spinal Circuits
Muscle = muscle fibres with membrane, attached to tendon
Lowest level of the hierarchy = motor unit = motor neurone and the muscle fibre(s) it innervates
The point of innervation = neuromuscular junction
Acetylcholine drives action at this level
Descending Motor Pathways
From the primary motor cortex, signals descend to the muscles through 2 dorsolateral regions in the spinal cord and 2 in the ventromedial region in the spinal cord
*Dorsolateral tracts
terminate in contralateral half of one spinal cord segment, and sometimes directly on a motor neurone

EXTRA NOTE: Dorsolateral- end in the contralateral part of the spinal cord- the opposite side- tracks from right cortex actually end up on the left side of the spinal cord and the body; sometimes attached directly to motor neuron; CONTROL LIMBS ARMS HANDS LEGS FEET

*Ventromedial tracts
more diffuse, with axons innervating interneurones in several segments of spinal cord body

EXTRA NOTE: they control the BODY or trunk
Dorsolateral tracts
Corticospinal tracts = DIRECT
Start form primary motor cortex and direct because make way directly down brain stem and spinal cord- pass through medulla and decussate- CROSS OVER TO OPPOSITE SIDE; end in dorsolateral part of spinal cord (back) and synapse again and control distal limbs- hands arms feet

Corticorubrospinal tracts =INDIRECT
Indirect= pass through red nucleus= decustate after brain stem and go down to the opposite side so dorsolateral cross over to other side of the spinal cord whether early or late

Few off shoots here; to control facial muscles in the indirect tract
If a lesion on right, left side effected etc.
Once crossed, end up in the same position on contralateral sides- controlling distal limbs
Dorsolateral summarized
Dorsolateral tracts control the movements of the limbs (hands, arms), and especially independent movement of limbs)

Lawrence & Kuypers (1968) transected dorsolateral corticospinal tracts in medullary pyramids of monkeys
After surgery, monkeys could stand, walk and climb
But could not use limbs for other activities (e.g. Reaching for things; and could not move fingers independently )
Ventromedial Tracts
Ventromedial Corticospinal
Direct down spinal cord and only once here that they send off diffuse connections to the other side
End in the ventral medial part of the spinal cord and control trunk and limbs close to the trunk (body)

Make way down but at the tectum and tegmentum make connections here and then are bilateral; feed into areas controlling cranial nerves and vestibular nuclei- important for sense of orientation- connections go to trunk and proximal muscles
Ventromedial summary
Ventromedial tracts: control of posture and whole-body movements, and they control the limbs movements involved in these activities
Lawrence & Kuypers (1968) transected ventromedial tracts
Monkeys had postural abnormalities
Impaired walking and sitting
Input from primary and secondary motor cortex
Feedback from motor responses from somatosensory and vestibular systems

gait (walking), speech and balance, and learning new motor sequences
fine-tuning and learning functions

Cerebellar ataxia

Lots to do with routine learning and also in navigation and in cognitive functions
Downward projections- take in info from sensory and motor cortex and feedback- as moving around, vestibular system is giving new information, all this is fed to the cerebellum and also taking in sensory information (touch hearing and vision) ALL THIS SI FED BACK TO CEREBELLUM
Gait= walking and rhythmic behaviors
Ataxia- lesion at this level, lack of coordination is seen in walking, and a wide based gait; legs further apart and stumbling
Basal Ganglia
Complex, heterogenous interconnected nuclei
They modulate movement
cognitive functions - habitual responses, implicit learning

Bunch of nuclei clustered together in the centre of the brain- each nucleus and structure in the basal ganglia is either inhibitory or excitatory- modulate each other in this way
This keeps motor control output very finely in tune but also cognitive function and routine habitual responses here
THIS IS IMPLICIT LEARNING- i.e. dancing or driving same route and cant even remember what actually happens the route or what happens basal ganglia took over
Basal Ganglia diagrammatic representation
powerpoint slide 13
Parkinson's diagramatic representation
powerpoint slide 14
Summary of interaction between basal ganglia and substantia nigra in Parkinson's
Direct and Indirect pathways
Depend on Dopaminergic connections from substantia nigra
Connections can be excitatory OR inhibitory: the output of one nucleus either excites (enhances) or inhibits (suppresses) the output of the next nucleus

FINE BALANCE between activation of these nuclei in the intact system
IMBALANCE in Parkinson's disease leads to extra or reduced movements
Parkinson's: positive symptoms
Positive= extra behaviors which did not previously exist
Patients may present primarily with
OR rigidity and akinesia
With/ without cognitive dysfunction, dementia, depression
Tremor- resting (disappears when limb is in use or in sleep- contrast with cerebellar intention tremor)
Rigidity- resistance to passive movements, leading to postural problems, loss of righting reflexes.
Rigidity + tremor may feel like "cogwheel rigidity" on passive movement by examiner
Forward leaning; backward leaning
Postural hypotension = many falls
Parkinson's : negative symptoms
Reduction in spontaneous movement (hypokinesia)
Slow initiation of movement (akinesia);
Progressive slowing or freezing during a movement and
Reduced range and scale of movement
Slow gait, often with freezing and small steps (marche à petit pas)
Rapid festinating gait
Poor arm swing
Postural instability = many falls

Dull, weak voice without inflections (hypophonia) and slow speech
Mask-like, unemotional expression
L-dopa and Parkinson's
L dopa- dopamine injection but this cant cross blood brain barrier but has to be in l-dopa format to do so

Side effects:
Disorientation, confusion
Auditory / visual hallucinations
Poor working memory
Dyskinesias at peak dose- poor movements, start to see extra movements and on off cycles- sometimes on and working well and then it flips
End-of-dose dysfunction
On-off cycles
Eventual drug failure
Huntington's disease
Huntington described the three peculiarities of the disorder:
- Hereditary nature Autosomal dominant with complete lifetime penetrance, chromosome 4; Autosomal dominant if you get gene from one parent you will get the disorder
- Manifestation in adulthood
- Tendency to 'insanity and suicide'
Huntington's cont.
Destruction of GABAergic (and some cholinergic neurones in striatum (caudate and putamen, and to some extent the globus pallidus)
Progressive striatal atrophy: Medial caudate first (small spiny neurones), then putamen, then tail of caudate
Defective metabolism precedes loss of tissue

SUMMARY: GABA connections and some acetylcholine in the striatum; progressive, starts form the end and goes to the main section of the striatum
Huntington's symptoms
First signs usually affective:
Depression, anxiety, irritability, impulsivity, aggression

Followed by:
Restlessness, clumsiness, poor coordination, forgetfulness and personality changes
Altered speech and writing, saccadic changes- changes in the functions of the eyes
Bradyphrenia and bradykinesia
Poor motor dexterity, unsteadiness, reduced speed
Athetosis, chorea
They often appear to be fragments of normal behaviours
They involve multiple joints and thus resemble voluntary action
They are briefly suppressible, and decrease during sleep
They increase with stress and with voluntary movements like walking
Quasi-undulating character is idiosyncratic to individuals
Intermittent tics
- motor
- verbal
Otherwise normal motor and sensory activity
Normal cognition

Partly suppressible
Anxiety increases
Sleep deprivation increases
Premonitory sensory phenomena

Genes, environment
Imbalance of GABAergic activity in basal ganglia (Leckman, 2002)
Management when severe: neuroleptics such as haloperidol and risperidone
BALANCE between excitation and inhibition
Not just basal ganglia,
Also cortical involvement
Primary motor cortex
In precentral gyrus of frontal lobe- Weakness is going to be contralateral to the effected area- opposite

Major hub of convergence of cortical motor signals
AND one of major outgoing point of signals

Damage: hemiplegia
Weakness (loss of power) in the body part represented by that site
Secondary motor cortex
Input from association cortex
Output to primary motor cortex
Consists of
preSMA- supplementary motor area
SMA- supplementary motor area
Dorsal premotor
Ventral premotor
3X cingulate motor areas (at least 2 in humans)
Programming of specific patterns of movement, with input from the dorsolateral prefrontal cortex
Sensorimotor Association Cortex - INPUT
Posterior parietal
Input from more than one sensory system
1. Integrates knowledge of (position of) objects and
2. Knowledge of position of body parts
3. Directs attention

Deficits after damage include ataxia and impaired body representation

Any information that you need to get you through that action happens here
Moves attention around the environment

Posterior parietal lobe major sensory hub so any information you need to get you through that action

Moves attention around the environment- ataxia and impaired body representation is nto knowing where your limbs are

Even higher 'CEO' in the system and the other area involves is the frontal eye fields so directing the eyes around the environment which is an important source of information

Apraxia and contralateral neglect
Damage to high level area act as if left side of space of body doesn't actually exist so contralateral neglect
Sensorimotor Association Cortex - OUTPUT
Posterior parietal
1. Dorsolateral prefrontal association cortex
2. Secondary motor cortex
3. Frontal eye fields

Deficits after damage include apraxia, contralateral neglect

This is the director: the decision making errors- in the decision to make an action
Not in the processing or action itself
Sensorimotor Association Cortex
Dorsolateral prefrontal
involved in the DECISION to make an action
- Not the action itself,
- And not in the processing of the target object(s)

- Input from posterior parietal cortex
- Output to secondary motor & primary motor cortex, and frontal eye fields
Inability to use visual information to guide movement of hands
- Deficit more severe in periphery of visual field
- Visual fixation preserved
Incorrect / awkward movements
Errors in accuracy (over/undershoots)
Inability to act, i.e., to move the moveable parts of the body in a purposeful manner

A disorder of skilled movement resulting from neurologic dysfunction

Presupposes ability to move is intact, and is not due to sensory loss, weakness or ataxia, or other movement disorder
Maintaining internal representations
Intrinsic spatial coding: knowing what our own body parts are doing

Intrinsic coding is essential when
a body part is going to be obscured from vision at some stage in the movement planning and execution

Superior parietal lobe is critical for sensorimotor integration by maintaining an internal representation of the body's state
Basic components of a motor control system and goal mechanisms
Powerpoint slide 43
The "Alien Hand Syndrome" diagram representation- alien hand is feeling as if hand does not belong to the body, have no control over the limb
Powerpoint slide 46
Summary of function of mirror neurons
William James: (1890): every mental representation of a movement awakens to some degree the actual movement which it is object"

Observing, imagining or in any way representing action excites the programmes involved in that action

If you imagine or watch a movement it activates the same part of the brain as if you were actually doing the movement

We are sensitive to other peoples actions, copying and there is some resonance between ourselves and other people
Action comprehension- understanding what they are doing
Mirror Neurones - the Action Observation System
Gallesse, Rizzolatti et al 1990s: mirror neurones in monkeys respond

1. to sight of goal-directed actions only
2. as long as the goal is achieved, even if it is out of sight
3. to sound of an action (multimodal)
4. when action is performed by an agent (hand-object interactions, not to tools) - ?????
Mirror Neurones - the Action Observation System CONT.
Premotor and parietal cortices activated by perception of action and execution; activation is greater when movements are to be replicated later

Mirror neurone system facilitates action understanding, allowing planning of our actions and understanding of others' actions
Mirror Neuron findings
Action GOALS, rather than action per se
Non-human models CAN elicit action obs effects
Context matters
Experience matters
Individual differences matter
Overview of the eye
Light enters through the pupil, but first it passes through the cornea (where the greatest amount of bending of light occurs) then passes through the lens- more of a fine tuning mechanism; for when you are looking from far to near and changes its thickness as a result of ciliary muscles.

Sensory membrane which contains light sensitive photoreceptors- distributed across the retina

Optic disk- where all axons from ganglion cells exit the eye; blind spot because no photoreceptors

Fovea- small in respect to the entire retina
Visual axis- to communicate where the eyes are looking at any particular point
Refer to powerpoint slide 2 for diagram
The Retina: Transduction of light into neural signals
The retina is composed of 5 layers:
From back to front:
Layer 1: receptors consisting of rods and cones
Layer 2: Horizontal cells
Layer 3: Bipolar cells (note that Ada and I discussed these cells in lecture one and two. They convey information in one direction only -- from the receptors on to the ganglion cells.
Layer 4: Amacrine Cells
Layer 5: Ganglion Cells.

Note that Horizontal cells and Amacrine cells are specialised for horizontal communication.

Obviously there are two problems with this design of the retina.
1) All the cells and axons are IN FRONT of the receptors!!
2) There is a hole in our visual field due to the blind spot where the axons from the ganlion cells exit the eye and proceed back to the thalmus.

The Fovea solves part of the problem of the retina being inside out.
The blind spot may not actually be a problem. The visual system perceptually fills in or erases parts of the visual field that are stationary for prolonged periods of time.

As light enters eye- passes ganglion, amacrine cells, bipolar and horizontal before rods and cone recepotrs- SO RETINA IS INSIDE OUT

The fovea is a solution to the "inside out" design of the retina.
The layer of cell bodies and axons thins out around this area of the retina.

Layers of cell have been pushed out of the way for the tiny part of the retina- the fovea- so light has a straight path here to the receptor cells ; 2% figure for fovea
Rods and cones- names reflect shape
Rod- far more numerous across retina and the cones are mediated for colour vision
3 types of cones;
At the fovea, cones far out number the rods- fovea only has CONES NO RODS
No photoreceptors=blind spot

Duplex retina- cone and rod system; cones are smaller than rods and packed in tightly particularly in the fovea and each cone gets a direct one to one connection right back to the visual cortex- directly to a neural unit in the visual cortex; high position acuity; neuron knows exactly what position on the retina it is coming from HOWEVER it takes a little bit more light to activate the cone; the cones are less sensitive to dim lights then rods; there is high convergence- hundreds of rods converge onto a single ganglion cells SO MANY RODS CONVERGE ONTO A SINGLE GANGLION CELL: DISADVANTAGE: WHEN THE NEURAL UNIT IN THE CORTEX IS STIMULATED, IT DOSENT PARTICULARLY KNOW THE SPATIAL LOCATION OF THE SIGNAL; UNCERTAINTY; but rods are much more sensitive to dim lights
Less sensitive but more spatial in cones and less spatial acuity in rods but more sensitive to dim lights
Visual Transduction:
The conversion of light energy into neural signals.
Photoreceptors contain pigment (e.g. rhodopsin) that responds electrochemically to stimulation by light.
Does not respond to neurotransmitters
Causes the receptor cell to hyperpolarize and release less neurotransmitter.
The bipolar cell, however, increases firing.

Change of physical energy into neural impulses; counterintuitive.

The photo pigment in this receptor is a g protein which responds to light so when light hits the molecule it changes its electrical properties- in the dark, the rod is slightly depolarised so it steadily releases a neurotransmitter to subsequent bipolar cells; glutamine is inhibitory neurotransmitter; when little light actively releasing and inhibiting NT to nerves so reduction in neural impulses

When light is absorbed by receptor it changes shapes and hyperpolarises receptor and reduces the release of the inhibitory receptor allowing the bipolar receptor connected to increase its fire so net result is an increase in firing becvaiuse the light si reducing the inhibitory connection between th receptor and bipolar cells
Cross section of the retina
Note that Horizontal cells and Amacrine cells are specialized for horizontal communication.

Horizontal cells and amacrine cells- the majority of connections are laterally cross the retina from left to right to facilitate horizontal communication

Tend to accentuate edges these connections- we want to be able to discern objects from the background, so a good visual system should accentuate edges; edge detection is a process that begins in the retina and allowed by these lateral connections
Horseshoe crab diagram
refer to powerpoint slide 12 and focus on my notes on the bottom
Axons from ganglion cells...
As the axons leave each eye they cross to the back of the brain- at the optic chiasm there is half crossing; half the axons from the left cross and join with half from the right

The most efficient way to process if the inputs from the two eyes joined up in the same neural coordinate in the cortex; a single location in space is processed by a single location in the visual cortex.

Things in the right visual field are processed by the left visual cortex and vice versa.

Lateral geniculate- one of the lobes of the thalamus- axons leave eye and first synapse occurs here; essentially a relay station and not much processing except that the wires or axons get matched up and organised nicely
Retinotopic organisation and the Cortical Magnification Factor
Adjacent locations ion the retina wire and connect to adjacent locations in the cortex- organisation is similar

The fovea is overrepresented in the visual cortex- cortical magnification factor; disproportionate amount fo cortical tissue dedicated to the fovea relative to other regions
Parvocellular and Magnocellular Pathways
The M and P Channels:
The LGN is composed of six layers.
Top 4 layers: parvocellular neurons (small cell bodies)
small receptive fields
- colour (cones)
- stationary objects
Bottom 2 layers: magno-cellular neurons (large cell bodies)
- large receptive fields
- achromatic (rods)

Parvocellular- small cells; cones, small detail and colour
Magnocellular- larger cells, rods, larger visual detail
6 layer structure- pathways start to get organised and top 4 layers of lateral geniculate constitute parvocellular neurons; mediates colour and stationary objects
Bottom two layers are magnocellular- see motion
The parvo and magno project on slightly different regions and this has follow on affects so they are processed in slightly different brain regions that are connected to the visual cortex
From the Retina to the Primary Visual Cortex
Four common feature of the three stages:
Fovea receptive fields smaller than the periphery
All receptive fields are circular
All neurons are monocular
Concentric excitatory/inhibitory regions

Receptive Fields:
Refer to regions on the sensory organ (i.e. the retina in vision) and the features that excite or inhibit the cell.
The nature of the receptive field of a cell gives clues about the cell's function.
Regions on the retina which excite or inhibit the cell so the nature of a receptive field of a cell gives clues to that cells function
Receptive field is a physical location on the retina that stimulates a particular cell in the visual cortex
Centre/Surround Receptive fields
Each receptor wires to a ganglion cell; any connections from these receptors on the retina has an inhibitory effect and depresses the firing rate of the cell
In the centre is a bunch of receptors to same cell except with an excitatory effect on the cell; so will either cause cell to fire vigorously or not
Most basic stage of image analysis in our system
When you aggregate this, conveys more and more complex information
Centre/Surround Receptive fields:
Sensitive to contrast.
Complete illumination of the centre maximises firing.

Complete illumination of the surround minimises firing

Diffuse illumination of the entire receptive field also minimises firing.

Stimulate center or surrounding, vigorous response of depression or excitation
If you shine light over entire receptive field, no change so cell is critically sensitive to RELATIVE STIMULATION- light in one region and not in the other
Receptors to Ganglion Cells to Simple Cells
If you aggregate information; each ganglion cells located in the eye; if you aggregate these cells to converge on another cell in the visual cortex, now you have a cell with a simple cell receptive field; bunch of excitatory regions lined up- so if we shine a vertical bar of light you would get a net excitatory response from these cells

If you moved it, you might get a net depression
Simple cell receptive field is more complex tha ganglion receptive field so simple cells tend to respond more vigourously to a vertical bar of light
Some simple cells...
Simple cells respond most vigorously when static bars with an appropriate orientation falls onto the "ON" subfield of the receptive field.

Here are some examples of simple cells. In all cases, the line, bar or contour must be stationary to elicit a response. REFER TO SLIDE 22

As with the centre - surround receptive fields, these do not elicit a response from diffuse illumination of the entire receptive field.
Single cell will respond to different positions etc.
Spatial frequency and gratings
It is possible to decompose and individual seem into spatial frequency components
Adding three sign waves gives us the bottom wave- you see that this wave form is more and more like a square wave
Sharp edges- represented by light dark edges on the visual field
Simple V1 Cells code spatial scale
SLIDE 24 for my extra notes
Low spatial frequency
Activates simple cells with widely separated subfields

High spatial frequency
Activates simple cells with less separated subfields

You would need a much larger receptive field to fire vigorously in response to this pattern in comparison to a smaller
i.e. inhibitory regions in the dark, so this receptive field will fire
We have different channels and pathways in the visual system that respond differently to visual components
Simple cells
Simple Cells: Coding for Spatial Scale
Signalling changes from light to dark at different spatial scales allows simple cells to code information about different features: edges and texture.

High spatial frequency information about edges

Low spatial frequency information about texture.
Complex Cells (V1, layers 1-3 and 5-6:
- fed by 2 SIMPLE CELLS
- This complex cell will fire if it gets ANY input from its contributing simple cells

Complex fields are comprised of numerous simple fields line up adjacent to one another
Complex cells will fire if the oriented conture falls anywhere within the field- so no excitatory or inhibitory fields
Fire more vigorously if contour moves through field
Many features of complex cells....DON'T NEED TO KNOW IN TOO MUCH DETAIL
Many complex cells are binocular -- they receive inputs from both eyes.
The cell will increase firing if inputs arrive from either the left or right eye.
More vigorous response if inputs arrive from both eyes simultaneously.
Some cells favour one eye over the other and respond more vigorously to one eye -- occular dominance.
Some cells respond well if similar contours fall on nearly the same positions in the two eyes -- that is they have a binocular disparity- what allows for 3 dimensional vision; vigorously sitmulating the complex cells bevause images falling on slightly
Columnar Organisation of the primary visual cortex
Signals flow from simple to complex
Functionally similar cells are grouped in columns in V1
Columns alternate in eye dominance

Orderly columnar organisation of simple cells- several layers of cells but each column will have cells that are similarly tuned that will respond vigorously to contures of the same variation; i.e. one column prefers an orientation of slightly off vertical
One column dedicated to left and adjacent to that a column dedicated to the right
Exploring within and across the cortical columns of V1
Take away point:
All neurons within particular column have a similar location and orientation in the opposite eye or column
Beyond the LGN and V1 to the Cortical Mechanisms of Vision and Conscious Awareness
Again, the major flow of information is from the primary visual cortex up to the different parts of the secondary visual cortex and onwards to the visual association cortex (major component is the posterior parietal cortex). This is some backward travel of information in the form of feedback.
As you travel up the processing chain, the receptive fields get larger and more specific about the types of patterns they respond to.
Cortical Scotomas
If you damage any portion of the visual pathway along to way you can introduce visual deficiencies
Scotoma- a blind spot, refers to a blind sport resulting from damage to the visual cortex
BUT we tend not to notice them
Is a condition where a patient's primary visual cortex has been damaged and a large scotoma is present.
Usually large - covering one half of the patient's visual field.
The patient reports no conscious visual perception within the scotoma.
Nevertheless, when tested, they perform above chance on many visual tasks.
- judging the orientation of lines they report they cannot see.
- correctly reaching for oriented objects
- correctly intercepting objects moving through their scotoma.
Two candidate explanations for Blindsight
Damage to the primary visual cortex is not complete and some residual functionality remains allowing the patient to perform above chance on some tasks.

Visual pathways exist that ascend to the secondary visual cortex without passing through V1. These pathways may support visual abilities without conscious awareness- ties in with ventral and dorsal processing streams
Two separate visual streams: what function do they serve?


Competing theories to explain the two visual streams; helps to refer to slide 38 for extra lecture notes
WHERE PATHWAY: could localise objects in space
WHAT PATHWAY - identifying objects and processing the specific features of objects

Modified original thought- people with damage to dorsal stream had difficulty locating objects BUT PROBLEM, when you ask something where something is it requires a motor response, so its not that it's a where system, but its really a visually guided behavior and that the what system is rather talking about conscious visual awareness

The patient with damage to the dorsal stream has problems with visually guided behavior but when you asked them to manually interact they were unable to do so; people with damage to dorsal where at chance with experimental chance
With damage to ventral stream, could manually interact but when asked to verbally report visual attributes she was unable
Prosopagnosia: a test of the visual pathway theory
A deficit in which the patient cannot recognise faces
In some instances not even their own.
Can distinguish between faces and other objects -- just not between faces.

There appear to be neural structures specific to faces.

TAKE AWAY: Appears to be neural structures specific to faces probably in the ventral stream
Prosopagnosia CONCLUSIONS
Provides an interesting test of Goodale and Milner's conscious awareness vs control of behaviour theory.

Prosopagnosia results from damage to the ventral stream - should impede conscious awareness but not control of behaviour.

Experiment on recognising familiar and unfamiliar faces.
- None of the faces were recognised.
- Familiar faces yielded heightened GSRs
- Therefore, evidence for the theory.

Summarized take away point: Participants were shown faces they knew but they didn't recognize it but skin response was also measured- familiar faces of family members yielded higher skin responses and took this as more evidence in response for ventral and dorsal streams- conscious visual awareness or visual guided behavior
So at this point I begin to realise how fooked i am because there is so muuuccchhhh :O lol
Communication can be defined as...
Behaviours used by one member of a species that convey information to another...

Gesture (body language)
Eye gaze control
Language can be defined as...
A communication system that has symbols (e.g. words) and rules for ways to assemble the symbols (e.g. grammar)
Aphasia can be defined as...
Defined as a loss of language processing ability after brain damage.

It is not...
An impairment of intellectual functioning
A psychiatric disturbance
A primary motor or sensory deficit
A developmental disorder
Classic views of aphasia
Three principles underlying classic aphasic syndromes (Caplan, 2003):

Localization of language processors
Damage to single processor can produce multiple deficits
Language processors localized because of relationship to primary sensory/motor functions
Classic views of aphasia CONTD.
Broca's aphasia (after Paul Broca)
non-fluent, expressive aphasia

Major disturbance in speech production
May retain some use of nouns & verbs
Loss of pronouns, articles, conjunctions ("telegraphic")
Comprehension intact

Speech is sounding clear
Disturbance in speech production retain some use of nouns and verbs but some loss of function words (joining words)
So speech sounds like a telegraph
Comprehension is intact
Spontaneous speech sample: Beach .... (5 sec)...man build....(4 sec).... sand... water .... Boat ..... Pier ... boy jump...
Broca's aphasia
In 1862 Broca concluded that the integrity of the left frontal convolution was responsible and necessary for articulation by examining his patient's brain lesion

MRIs of Tan's brain show lesions extend into the deep white matter including insular cortex and basal ganglia
Classic views of aphasia CONT.
Wernicke's aphasia (after Karl Wernicke)
fluent, receptive aphasia

Major disturbance of auditory comprehension
Fluent speech, normal rate, rhythm, intonation
Disturbances of sounds, structures of words
Semantic substitutions or paraphasias
Poor repetition, naming

Understanding and receiving language
- Speech sounded fluid- normal rate and rhythm, normal intonation
But disturbance in structure of words and sounds- say wrong word which means something similar- same category of items
More repetition and naming

The man is building the cake on the shore. There is a lot of water that is washing over the object that carries people over the water. In the back is the little houses that are used to change into the materials that are used when you want to go into the water.
Wernicke's aphasia
1874 wrote "Der aphasische Symptomenkompleks"

Documented the localization of the 'storehouse of auditory word forms' in the posterior portion of the left superior temporal gyrus
Classic views of aphasia
Conduction aphasia (Wernicke again)
Disconnection syndrome: disruption of arcuate fasciculus (white matter tract between Broca's and Wernicke's areas)

Failure to repeat
Paraphasias (phonemic)
Lichtheim's (1885) house model
Slides 16- 20
Classic views of aphasia: Transcortical sensory aphasia
Transcortical sensory aphasia
Disconnection syndrome: disconnection of auditory and concept centres; damage to tracts in temporo-parietal-occipital junction

Disturbance of auditory comprehension
Semantic paraphasias
Fluent, grammatical speech
Good repetition

Disconnection- damage between two main centers
Damage in connecting tracts in temporal parietal regions- back of brain
Semantic- instead of saying chair they might say table; same category of furniture but come out with the wrong item
Fluent speech, repetition is good
Auditory comprehension- have trouble understanding what you are saying in order to respond appropriately; they can talk and are fluent but not related to what you are asking or saying
Classic views of aphasia: Transcortical motor aphasia
Transcortical motor aphasia
Disconnection syndrome: disconnection of concept centre from motor and auditory language centers, lesion to tracts superior and/or anterior to Broca's
Intact auditory comprehension
Good repetition
Severe disturbance in initiating responses (adynamic)
Frontal dynamic aphasia

Tends to be more anterior- damage in the left frontal lobe or more in the frontal region
Tend to understand can mostly repeat but severe disturbance in initiating responses
Frontal dynamic aphasia- have normal language; if you had a pen and say what's this they say it's a pen and they can repeat the word pen and you ask them to read it and they know how to use it; they have normal language but do not use it voluntarily or at will to communicate
What's wrong is what she is thinking and what she is selecting to say- when we limited the options and decreased the selection load, the patient could speak and talk
Problem with initiating speech in terms of a selection deficit; they have a very clear cause
Summary of classic aphasias
Psycholinguistics and aphasia
Classic aphasic syndromes have limitations

Poor classification of patients- not all patients clearly fit one category

Lesion overlap/variability- not always lesions in corresponding areas of the brain

Little assistance for treatment planning; primary progressive aphasia (a typical dementia where language is the first presenting symptom- trouble getting out names of items, semantic dementia (loose understanding of what things are) (i.e. if someone is mute, knocked out several aspects?) ; eg. A little conduction, a little Wernicke's- hard to devise treatment plan based purely on one of the names; it's a good starting point and communicating at a basic level but it doesn't tell you want to treat
Psycholinguistics and aphasia CONTD.
Psycholinguistics does not view language in terms of production and comprehension

Emphasises language processing operations:
Phonology: sounds that compose language and the rules that govern their combination
Semantics: words and their meaning
Syntax: methods for combining individual words to convey propositional meaning
Psycholinguistics: Phonology
Two ways to represent sound in speech:

Phonetic: how phonemes are produced in different contexts e.g., the difference between English and French pronunciation
International phonetic alphabet (IPA)

Phonemic: smallest unit of sound that can signal meaning (e.g., /b/ in /bat/ and /p/ in /pat/);
In English: lips, slip, spill, pills, and lisp comprise the "same sounds" in different orders
Psycholinguistics: Syntax
Broca's aphasics have difficulty with syntactic production:
Few function words (e.g., verbs) are produced
Content words preserved (telegraphic speech)
Evident in spontaneous speech, repetition and writing.

We now know that these anterior lesions are also associated with comprehension deficits...

Agrammatic aphasia
Production and comprehension are impaired, although deficits are dissociable.

Sentence: "The girl the boy is chasing is tall"
Question: "Who is being chased?"

Broca's patients have trouble answering

Wernicke's aphasia patients usually do not have difficulties with syntax.
Psycholinguistics: Semantics
Word meaning and lexical form are represented separately

Lesions resulting in double dissociation of lexical and semantic representations of words:
Intact semantic knowledge, impaired naming = 'Tip of-the-tongue' & anomic deficits
Intact naming, impaired semantics = anterior temporal lobe atrophy (semantic dementia).

Lexical form in the house is A whereas the content is C
When they cant get the name of think about it on the spot- tip of the tongue
When you don't have the concept- semantic dementia; not that memory of events is bas but have difficult with knowing what things are and have difficulty with getting the right name out ; THIS IS AN ANOMIC DEFICIT

Semantic processing relatively spared in anterior lesioned (Broca's) aphasic patients.

Posterior lesions (Wernickes) are more often characterized by semantic impairments

Problems arise for anterior lesion patients when syntax is important in sentence comprehension (e.g., "Place the blue circle on top of the big red square"
Psycholinguistic vs Classical
Classical characterisation of aphasic deficits:
Broca's = poor speech production
Wernicke's = poor speech comprehension
Dissociation: comprehension vs. production

Psycholinguistic characterisation:
Anterior = syntactic processing
Posterior = semantic processing
Dissociation: syntax vs. semantics
Alexia and agraphia
Impairment in the ability to read or loss of ability
Subtypes: surface, phonological, deep

Impairment in the ability to spell or write

Alexia without agraphia

Joseph Jules Dejerine (1891/1892)

Two patients with left parietal lesions
One with poor reading and writing
Alexia with agraphia
Disturbance to the 'optical images for words'
Second patient with poor reading and preserved writing
Alexia without agraphia (i.e. pure alexia)
Alexia and dual routes to reading
Phonological route to reading - convert letter strings to sounds understand the meaning (grapheme-to-phoneme)
If damaged - phonological alexia

Direct route - printed words are directly linked to meaning in a visual form system
when reading irregular words, such as "yacht" or "colonel" or "pint"
If damaged - surface alexia

1. PHONOLOGICAL- Converting sounds together to get a whole word and then you understand what it is- written to sound form; if you are reading a fairly long word, you have to convert each individual grapheme to a sound then put it together- fi this is damaged, phonological alexia

Direct route- look at word, map it to meaning and that allows you to say the word out loud, route you need if you are reading irregular words- many graphemes do not map directly; so if you cant just look at the word and map the whole word onto meaning you are going to make errors- surface alexia; sometimes you have to know the word to pronounce a word properly
Inability to write or spell while writing

Central dysgraphia refers to problems accessing orthographic information from lexical stores or from applying sound-to-spelling phonological rules (dual route)
Peripheral dysgraphia reflects distortions in writing or typing (motor programs)

- Central- means problems to the actual processes involved in spelling; problems with accessing written form
Micrographic- someone notices that their writing is becoming smaller; characterised by movement or motor problems
Outline of memory
Explicit memory- being able to declare what we know, be conscious of information to be able to tell other about it
Implicit- riding a bike, at first not without effort and somehow you encoded that procedure to where now you just ride; don't declare, aren't conscious of steps involved, comes with practice
Sensory memory
Lasts only a few milliseconds

like an 'echo'; can be retrieved if the attempt is made fast enough
Sensory memory trace:
Iconic/visual (retina, primary visual cortex)
Echoic/auditory (cochlea, primary auditory cortex)
Short term memory
Donald Hebb (1949) proposed that there are two types of memory:

Short-term memory (STM) - memory of events that have just occurred.

Long-term memory (LTM) - memory of events from earlier times.

STM has limited capacity.
Lets you remember a phone number long enough to call it, but decays quickly without rehearsal. Cues don't help. (e.g., 78253149).
"7 plus or minus 2 items"

Domain (or type of material)
Auditory-verbal "phonological loop"
Visuospatial sketchpad
Working memory
The temporary storage of information while we actively attend to it or work on it...

A test of working memory is repeating a set of numbers backwards (e.g., 782531 - 135287) the delayed response task. It requires a response to the same stimulus as that presented a short time earlier.

Lesions to prefrontal cortex impair performance.
Learning and Long term memory:
Evidence from list-learning tasks

List of 15 words, repeated 5 times, SAME ORDER
S repeats the list (A) after each time (rehearsal)
A distractor list B of new words is given ONCE
The S is asked to recall List B then the 1st List A
After a delay ~20min, S asked to recall List A again, then they are asked to recognise the words from a larger list.

Evidence from list-learning tasks
Retrieval effects:
free recall, cued recall, recognition
Free recall- no help, simply recall- it is harder than other types
If there are some clues given, might trigger or help retrieve information- cued recall
Recognition is easier- list with extra items, most would recall what wasn't on the list
Declarative memory
Episodic memory
Memory for a specific event and the context in which it occurred.
What happened, where did it happen, etc.

Semantic memory:
conceptually-based knowledge/facts about the world (people, places, objects, words)
Declarative memory: Patient H.M.
Bilateral medial temporal lobe resection at 29 y.o. to treat intractable epilepsy

After surgery, demonstrated memory difficulties:
Reported his age as 27
Could not remember people minutes after meeting them
Could not form new long-term memories

Biographical knowledge up to the time of the surgery was intact (1953)

Studies on H.M. generated five main findings (Eichenbaum ,2013):
memory is a distinct psychological function,
amnesia spares short-term and working memory,
amnesia is an impairment of declarative and episodic memory,
the hippocampus is a core brain structure supporting memory,
the hippocampus supports the permanent consolidation of memories
Declarative memory: Amnesias
Anterograde ("going forward") amnesia
inability to form new memories after the brain damage occurred.
vs. Retrograde ("old memories")

HM has massive anterograde amnesia after the surgery.
Anterograde amnesia
Anterograde ("going forward") amnesia

Also observed after diencephalic lesions
Thalamus, hypothalamus and pretectum
Retrograde amnesia
Retrograde ("going backward") amnesia
loss of memory for events before the brain damage.

Patient KC
motorcycle accident (age 30). Severe TBI and subdural haematoma was removed
severe anterograde AND retrograde amnesia after the surgery.
Declarative memory: Patient KC
Damage to medial temporal lobe (almost complete hippocampal loss), frontal, parietal and occipital cortices
IQ 94
Language normal
Good reasoning and concentration

Retrograde amnesia involved info from entire life
No recall of personally experienced events, though could recall facts. Could learn new info, but could not recall how he acquired it.

Despite this, he had intact semantic memory for general world knowledge acquired prior to accident (e.g., difference between stalactites and stalagmites)

Episodic and semantic memories are dissociable
Declarative memory: semantic
Semantic memory:
conceptually-based knowledge/facts about the world (people, places, objects, words)

3 contemporary classes of theory
Distributed-plus-hub (or -plus-convergence zones
Embodied cognition
Semantic memory
Distributed models do not localise semantic memory to any particular structure

Distributed-plus-hub models propose a key role for the anterior temporal cortex in mediating abstract conceptual representations (semantic dementia)

Embodied or grounded models propose meaning is represented in the same sensory or motor structures responsible for mediating perception and action
Non-Declarative memory
Procedural memory

ability to develop motor skills (remembering or learning how to do things, e.g., riding a bike).

Patient H.M shows intact procedural memory

Evidence for dissociable memory systems

Patient H.M shows intact procedural memory
Mirror tracing task
Performance improved over 3 days
Could not remember performing the task

Perceptual priming
Determining objects from fragments
Patient H.M.'s performance improved
Could not remember performing the task
Summary for memory!
Sensory, STM and LTM
Declarative memory
Anterograde and retrograde amnesias
Role of the media temporal lobe
Non-declarative memory
Procedural memory, conditioning
Evidence for dissociable memory systems