midterm 2 Flashcards
1
Q
what is functional segregation?
A
each level of sensorimotor hierarchy is composed of different units
2
Q
sensory feedback
A
- sensory systems monitor body responses
- feed info back to sensorimotor circuits
- many adjustments that occur via SM feedback occur by unconscious mechanisms
- are carried out by lower levels of hierarchy (eg. spinal circuits)
3
Q
ballistic responses
A
brief, all or none, high speed movements (sensory feedback is not involved)
4
Q
main assertions of SM program theory
A
- LL of SMH possess sensorimotor programs that represent particular patterns of activity
- a particular complex movement is produced by activating combinations of these programs
- once particular level is activated, it can operate on basis of sensory feedback without direct control by higher level
5
Q
motor equivalence
A
most movements can be carried out in a variety of ways (can produce same movement through different effectors)
EX: signing name with toes in the sand rather than using hand
6
Q
what are the implications of having motor equivalence
A
indicates that SM program codes are independent of limb representation
the name signing motor program must be held at higher levels of SMH (?)
7
Q
processes that influence learning of SM program (practice)
A
- response chunking = carrying out motor programs as chunks rather than individual units
- EX: typing “Vancouver” as a smooth set of movements
- shifting control to lower levels
- frees up HL for more esoteric aspects (eg. focus on the expression of musical performance rather than individual notes)
8
Q
unconscious processes (circle illusion)
A
although people perceive the circles as different sizes, their SMS responds in an unconscious pattern as if they are the same
EX: they will open hand to same degree when asked to reach out for the circles
9
Q
two major areas of SM association cortex
A
- posterior parietal association cortex
- dorsolateral prefrontal association cortex
10
Q
function of posterior parietal association cortex
A
integrates info about current position of body parts with info about positions of external objects you wish to interact with
a mosaic of areas responsible for guiding movement
11
Q
what is the somatosensory cortex
A
area of the parietal lobe
- controls eye movements
- implicated in attentional mechanisms (eg. visual selective attention)
12
Q
Desmurget et al (2009)
A
- studied people who were undergoing neurological surgery for brain tumors
- when mild stimulation to various areas of posterior parietal association cortex, patient formed intention to perform particular actions
- greater intensity: felt like they had already performed those movements
13
Q
lesions to posterior parietal association cortex
A
deficits in perception and memory of spatial relationships, accurate reaching and grasping, control of eye movement, attention
Apraxia (left side) and Contralateral Neglect (right side)
14
Q
Apraxia
A
a disorder of voluntary movement that is not attributable to a simple motor deficit
- difficulty making specific movements (eg. artists would be able to paint on canvas but difficulties on an uncommon surface)
- damage is unilateral to LEFT posterior parietal lobe but symptoms are bilateral
- language production deficits are common
15
Q
domains of action susceptible to apraxic errors
A
- imitation of gestures (especially meaningless ones)
- performance of meaningful gestures on command
- real or pantomime use of tools and objects
16
Q
Goldenberg (2008)
A
showed there is actually only one domain that is reliably susceptible to apraxic errors => imitation of meaningless gestures
17
Q
Contralateral neglect
A
due to large lesion to or dysfunctional activity in RIGHT posterior parietal lobe
- viewer-centered: unable to respond to stimuli to the left of their body (posterior parietal cortex)
- eyes tilted to the right
- actions are focused on the right (eg. not shaving left side of face)
- object-centered: unable to respond to left side of objects (superior temporal gyrus)
18
Q
evidence that (contralateral) neglect is not complete
A
- when object is repeatedly presented at the same spot to the left, patients begin to orient to that spot even though they are otherwise unaware of
- patients are better at completing an incomplete drawing to their right if the complete version of the drawing is first presented to their left
19
Q
function of dorsolateral prefrontal association cortex
A
involved in evaluation of external stimuli and initiation of voluntary reactions to those stimuli
- neurons in dorsolateral prefrontal cortex fire first
20
Q
secondary motor cortex (input and output)
A
- receives input from association cortex
- sens output to primary motor cortex
- there are multiple secondary motor cortices
21
Q
general function of secondary motor cortex
A
in general:
- involved in programming of specific patterns of movements
- takes instructions from dorsolateral prefrontal cortex
Electrical stimulation: elicits complex movements (often bilateral)
recordings: neurons become active just prior to initiation of a voluntary movement
involved in complex series of movements and mental rehearsal of those movements
22
Q
mirror neurons
A
fire when individual performs a particular goal-directed movement or when they observe that movement performed by another individual
23
Q
Rizzolatti (1990)
A
neurons in monkeys fired just as robustly when monkeys observed research move an object
neurons also fired when the placing was behind a screen (neurons fire NOT because of visual input but the understanding of what action is to be performed)
24
Q
primary motor cortex conventional view
A
GENERAL : each site in PMC controls a muscle in the contralateral part of the body and each neuron produces movement of that body part in a particular direction
STIMULATION : (Penfield somatotopic layout of primary motor cortex)
- each area when activated produced contralateral muscle activation and a very simple movement
RECORDING : each neuron is movement direction-selective (ie. fires most rapidly to movements in one particular direction)
25
primary motor cortex (current view)
uses longer bursts of higher intensity current to match recorded motor responses
movements that resulted were not the muscle twitches or segregated joint rotations that Penfield observed
they were complex, involved coordination of many joints, and resembled meaningful actions
ie. there is no clear demarcation of where a certain part of the PMC is responsible for a certain pattern of actions — no clear demarcation of where one begins and the other ends
26
PMC (current view) : end point vs direction
If a particular PMC site is stimulated, the body part will reach the same end point regardless of its start position.
If monkeys performed natural body movements, firing of many primary motor cortex neurons was most closely related to END point of the subsequent movement not the direction
when stimulations were applied, elicited hand movements were roughly equivalent in frequency to what was observed during spontaneous activity
27
possible effects of damage to cerebellum
* loss of ability to precisely control direction, force, velocity, and amplitude of movements
* loss of ability to adapt patterns of motor output to changing conditions
* difficulties in maintaining steady postures (eg. standing)
* disturbances in balance, gait, and the control of eye movement
* impairments on measures of attention and executive control, procedural memory, working memory, language and visual-spatial processing
* impairments in the learning of new motor sequences.
28
what are reverse prism goggles used for
to check for **damage to cerbellum**
task: individual wears reversing prism goggles and throws darts
if there is damage to cerebellum:
* marked impairments in ability to adjust to goggles over time
* return immediately to baseline after taking off goggles (ie. shows no adaptation to prism goggles)
29
current views of cerebellar function
1. plays fundamental role in **timing**. when damaged, motor commands and cognitive states are no longer appropriately selected and sequenced
2. cerebellum is involved in **sensorimotor imagery** (it is active during imagined and real actions)
3. it is a **learning machine**: supports the adaptive plasticity needed for the emergence of skilled behaviour
30
basal ganglia
group of complex interconnected nuclie that performs modulatory functions
are part of a neural loop that received **cortial input** from various cortical areas and transmits them back via **thalamus** to various areas of motor cortex
31
evolving views of basal ganglia function
**traditional view**: modulate motor output
**current views:**
* also involved in variety of **cognitive functions**
* promotes **new skill learning**
* acts as a tutor for the cortex to help **consolidate new skills**
32
initial symptoms of PD
(mild) slight stiffness and tremor of fingers, develops on one side and down legs, eventually becomes bilateral
33
symptoms of full blown PD
* tremor that is most pronounced during inactivity but not during voluntary movement or sleep
* muscle rigidity
* difficulty initiating movement
* slowness of movement, mask-like face
* pain and depression
* REM sleep behavioural disorder : act out dreams (ie. no suppression of motor movements)
34
4 cardinal motor symptoms of PD
1. tremor at rest
2. bradykinesia (slowed movements)
3. rigidity
4. postural instability
and also motor issues: inability to move past discontinuous patterns on the floor that creates a mental boundary
35
early warning signs of PD
1. diminishing sense of smell
2. sleep problems (vivid dreams, REM sleep behaviour disorder)
3. depression
36
mechanism of PD
**degeneration of neurons in SN — nigrostriatal pathway**
* by the time motor symptoms appear, 50-80% of cells already died
* most cell loss is in SN but that is not the only affected area
37
role of Lewy Bodies in PD
**Lewy Bodies** = clumps of protein that are found in the *surviving neurons of the SN* (but are also in other areas of the brain)
* LBs are also present in *dementia with LB* and some cases of *Alzheimers*
* In Parkinsons with Dementia (PDD) you see 10 times as many LB in cortex than in SN
* cortical LBs are best predictor of dementia in Parkinsons
38
Etiology of PD (Who gets PD)
* about 0.5% of the population develops PD
* likelihood of development increases with age
* more likely in males than females
No obvious cause but may be related to
1. gene mutations to a-syn or parkin
2. environmental causes like exposure to chemicals (eg. paraquat herbicide, maneb fungicide, rotenone pesticide)
been shown that injecting animals with these chemicals over time will result in PD (rats are resistant but not primates)
39
PD drug treatment (L-Dopa)
**L-Dopa** = precursor to dopamine which can get across the blood-brain barrier which the brain can then convert to dopamine
Major issues with L-Dopa
* **dyskinesias** = wavy action due to inability to control muscles
* 'wearing off' phenomenon
L-Dopa has short half-life (2-3h) so must take often throughout the day
40
PD treatment : Deep-Brian stimulation
low-intensity, high-frequency electrical stimulations to the **subthalamic nucleus**
seems to lose efficacy over time
pacemaker is used similar to treatment of epilepsy
41
MPTP model of Parkinsons
**MPTP** = methyl phenyl tetrahydropyridine
* MPTP can be accidentally produced during the synthesis of recreational drup MPPP
* MPTP targets domanine neurons: MPTP is converted to **MPP+** which is then taken up by the dopamine transporter
42
epilepsy characteristics
characterized by **recurrent unprovoked seizures** due to atypical, excessive or synchronous **neuronal activity** in the brain
43
diagnosis of epilepsy
* diagnosis of epilepsy relies heavily on the EEG
* interictal spiking has specificity of 97% but low sensitivity
**convulsion** = behavioural manifestation of seizure
**seizure** = electrical activity measured using EEG
44
stages of seizures
ictal = during seizure
interictal = between seizure
postictal = immediately after seizure (often when depression occurs)
45
importance of epileptic aura
1. the nature of aura is predictive of epileptic focus
2. they warn the person with epilepsy of an impending seizure
46
categories of epilepsy
**focal seizure** = does not involve the entire brain. Usually localized to a single brain area
**simple partial**
* symptoms are primarily sensory or motor or both, no loss of consciousness
* eg. twitches on a particular body part, tonic extension (muscle contraction) on one side of the body
**complex partial** (most common)
* engage in compulsive, simple behaviours (automatisms) and more complex behaviours that can appear perfectly normal (eg. turning head to one size)
* disruption/alteration of consciousness: often remember experience in "dreamy state"
**generalized seizure** = involves the entire brian
**absence**
* no significant convulsion
* primary symptoms: loss of consciousness (unaware of it), cessation of ongoing behaviour, vacant look, fluttering eyelids
**tonic-clonic**
* loss of consciousness and eqi, convulsion, tongue-biting, urination, cyanosis (turning blue)
* muscle contraction + rhythmic movement
* should ease person to floor, turn on side, remove accessories
* longer than 5 mins = "status epileptic" and needs anti-convulsant otherwise brain damage and break bones
**secondary generalization** = when focal seizure evolves into a generalized seizure (can happen within a seizure or over lifespan when focal is left untreated/becomes repetitive and worsens)
47
suspected etiology of epilepsy
1. genetics
2. infection
3. injury
4. cryptogenic = we don't know where it came from
5. idiopathic = people who don't respond to treatment
48
spectrum of seizures
immediate seizure = within 24h after any kind of brain injury
early seizure = less than 1 week
late seizure = more than 1 week
latent period = time between injury and onset of late seizures
49
general mechanisms/progression of epilepsy and seizures
1. brain injury
2. repair (no seizure) // early seizure
3. endogenous repair systems
4. epileptogenesis (process by which epilepsy develops) continues or stops
5. if develops then reaches onset of epilepsy and it either progresses or doesn't
ictogenesis = process by which seizures develop
*the more plastic the brain/brain part is, the more epileptic prone (ie. hippocampus is most prone*
50
epilepsy comorbidities
people with epilepsy are more likely to experience:
* diabetes
* depression and anxiety
* migraine headaches
* stroke
* heart disease
* asthma
* arthritis
51
epilepsy treatments
**1. anticonvulsants**
side effects: mixed bag od side effects (eg. memory)
* can also work as medication for other disorders such as depression, anxiety, or pain
**2. ketogenic diet**
* high fat, med protein, low carbs
* can reduce symptoms in children by 50%
* body stops relying on glucose and shifts to ketone bodies
**3. vagus nerve stimulation**
* modulate stress response though vagal stimulation as stress is a cause of epilepsy
*for sever intractable epilepsy, surgical procedures are sometimes required—focal removal of epileptic part of the brain (not possible for absence seizure)*
52
streams of visual information
visual info transmitted from primary visual cortex to visual association cortex via:
1. **dorsal stream** = V1 — dorsal prestriate cortex — posterior parietal association cortex
2. **ventral stream** = V1 — ventral prestriate cortex to inferotemporal cortex
53
damage to visual streams
**inferotemporal cortex** (what pathway) = no difficulty reaching for objects but have difficulty describing
**posterior parietal association cortex** (where path) = have difficulty reaching accurately for object but have no difficulty describing them
54
Milner and Goodale (DF)
DF had bilateral **ventral-stream** lesions
* profound visual form agnosia
* couldn't discriminate between two blocks of different sizes/orientations but could accurately reach for them (ie. knows how to appropriately interact with objects)
55
Milner and Goodale's differentiation between dorsal and ventral stream
they argue that the difference is not the kinds of information they carry but the use to which that information is put
**dorsal stream** = direct behavioral interaction with objects (action)
**ventral stream** = mediate conscious perception of objects (perception)
56
agnosia
"lack of knowledge"
* loss of ability to **recognize** objects, sounds, and shapes with
* no evidence of significant memory loss
**Types of agnosia:**
* form
* motion (see everything as frozen snapshots)
* colour
* figure vs ground (ability to distinguish between an object and foreground/background)
* faces
* language
57
apperceptive agnosia
failure in recognition linked to **problems in perceptual processing**
* unable to match **unusual views** of an object
* ability to recognize **degraded stimuli** is impaired
* often better with **local vs global** aspects of an object
* in severe cases, find it difficult to copy objects or shapes
58
associative agnosia
normal representations but unable to use this information to recognize things (ie. pure agnosia)
* there is no connection between incoming perception and existing knowledge
* know what a cow is and what its features are, but unable to identity a cow when presented with one
* do well on perceptual tests but cannot access names or other information about objects
* fails to experience familiarity with stimulus
* can give accurate verbal descriptions of an object with given the name
* can copy objects accurately but cannot tell you what they are
* no problem naming faces, just objects
* can imagine an object in their mind and draw it out vividly but cannot recognize their own drawings
* can recognize objects through other methods (eg. touch)
59
prosopagnosia
failure of face recognition
* can describe the characteristics of a face but cannot recognize whose face it is (recognize that they all have different faces but none of those faces look like anyone)
* a **selective visual deficit** and usually occurs in the absence of any other visual impairment, cognitive deficit, or psychiatric illness
For acquired prosopagnosia:
**retrograde component** = affects previously familiar faces
**anterograde component** = affects newly experienced faces
*symptoms are less severe when it is congenitally acquired*
**Skin Conductance Response**
* sensory detector is attached to the person
* they show sensory reaction to the faces of people they know
**Capgras delusion** = feeling like family members are imposters (couldn't tie feeling of recognition to the things they see even with pets/objects)
* show less skin conductance response when presented with familiar objects
59
fusiform gyrus // fusiform face area (FFA)
highlighted by PET and fMRI as an important region of the **ventral temporal lobe** in the processing of faces
* later work identified occipital face area (OFA) as being critical for face processing
* FFA is now thought to be important only for discriminating faces from other objects
60
prosopometamorphopsia
visual disorder characterized by altered/distorted perceptions of faces
61
attention (spatial)
implies withdrawal from some things in order to deal effectively with others
spatial attention : supported by a network largely in the **frontal and parietal cortices** of the **right hemisphere**
62
anosognosia
you don't know what you don't know
* common in neurological disorders (eg. schizophrenia) following brain damage where patients are unaware that they have a condition
Eg. contralateral neglect (usually disappears on its own after some period of time)
63
treating contralateral neglect
1. prism goggles
* goggles shift their vision 10º to the left
* their drawings improve more quickly with goggles as if draws attention to details in their left visual field
* speed of adapting to prism goggles is faster if they can interact with objects around them
2. mental imagery
* time intensive training (50 1h sessions)
* "imagine doing something with the left side" or "imagine the left side of space"
3. TMS
* low frequency repetitive TMS applied to the **left posterior parietal cortex** (the non damaged side) reduces symptoms of neglect but only temporarily
64
Case of HM
received **bilateral medial temporal lobectomy** : removal of medial portion of temporal lobes including **hippocampus** and **amygdala**
**retrograde amnesia** = inability to retrieve memories for some limited time prior to brain damage
**anterograde amnesia** = inability to form new memories of events after brain damage
**Short vs long term memory**
* digit span test (short-term memory) : intact
* digit span +1 test (long term memory) : impaired
* couldn't repeat more than 8 digits after 25 trials
**Long-term memory**
* explicit: episodic (involves time and place) or semantic (knowledge and concepts)
* implicit: procedural (skills and action), conditioning (HM was susceptible), priming (eg. incomplete drawing test)
*people have selective loss of either/both of episodic and semantic*
**explicit vs implicit memory**
* tested using mirror drawing test
* HM's performance improved over time even though he had no recollection of performing it
* improvement => intact implicit memory (procedural/not conscious eg. muscle memory)
* lack of memory for sessions => deficit in explicit memory (declarative/conscious)
HM can draw the layout of his old house and has familiarization with his own face suggesting that his **episodic memory** is in tact
65
Korsakoff's syndrome // Wernicke's syndrome
attributable to brain damage that results from **thiamine (vit B) deficiency**
* thiamine deficiency is often due to prolonged heavy alcohol consumption
* syndrome involves severe anterograde and retrograde amnesia, motor problems, extreme confusion, personality changes
CASE STUDY : Hiroshi
* cannot remember that he cannot remember
* cant recognize himself in the videos
* events that are connected to strong emotions will stay with him for longer
* still has concept of language (ie. semantic memory intact)
**medial diencephalic amnesia** = damage to thalamus + hypothalamus + mamillary bodies (sometimes)
66
Etienne-Jean Georget
raised the concept of irreversibility of the dementia process
67
common dementias
* Alzheimer's disease (60%)
* vascular dementia (20%) : due to multiple smaller ischemic infarcts, high blood pressure and cholesterol issues leading to mini-strokes
* dementia with LB (5%) : LB predominantly in cortex
* Fronto-temporal dementia (2%)
* Parkinson'd disease with dementia
68
history of alzheimers
post-mortem analysis of pre-senile dementia patient reveals presence of: **senile plaques** (amyloid plaques) and **neurofibrillary tangles**
69
AD symptoms
* early symptoms: selective declines in memory
* later symptoms: confusion, irritability, anxiety, and deterioration of speech
* advanced stages: difficulties with even simple responses (eg. swallowing, bladder control)
70
general types of AD
1. early-onset AD
* diagnosis before 65
* 5-10% of all cases
2. late-onset AD
* diagnosis after 65
* 90-95% of cases
*note that there is no difference in the neuropathology of the two types*
3. mild cognitive impairment (MCI)
* cognitive symptoms that precede AD diagnosis
71
memory decline in AD
**first signs**
* short-term memory loss
* prospective memory loss (ability to remember to do something)
**early**
* memory for new facts or episodes selectively affected
* less so: memory for older episodes, semantic memory, implicit memory
**medium**
* long-term episodic memory begins to be affected
72
three defining characteristics of AD
**1. Neurofibrillary tangles (tau)**
**2. Amyloid plaques (beta amyloid)**
* proteins fold when forming and amyloid plaques occur from misfolding => sticky form that clumps together and also clumps to neighboring cells
**3. substantial decrease in brain volume**
* mainly due to loss and shrinkage of neuronal processes (synapse loss) but also due to loss of neurons
73
biomarkers of AD
1. **low beta-amyloid levels** in cerebrospinal fluid (because they are clumped somewhere else)
2. **high tau levels** in cerebrospinal fluid
3. decreases in **hippocampal volume** (MRI)
4. decreases in **brain metabolism** (FDG-PET)
5. **Amyvid** (a radioactive marker that binds to beta-amyloid) and PET
6. suggestions of potential **blood test** for beta-amyloid
74
theories of pathogenesis in AD
1. amyloid cascade hypothesis = starts with misfolding of beta-amyloid
2. neurofibrillary (tau) hypothesis = starts with high levels of tau
3. inflammatory hypothesis (microglia)
75
diet compounds with antioxidant and epigenetic properties
*ie. can be protective against Alzheimers*
* reservatol, caffeic aid, selenium etc
76
current treatments of AD
1. **acetylcholinesterase inhibitors** to improve cognition
2. **NMDA-Receptor antagonists** are believed to limit neurotoxicity and they seem to improve cognition
3. the drug **aducanumab** was approved for the removal of amyloid plaques but the efficacy is unclear (it is an amyloid beta-directed antibody)
4. **SSRIs** for symptoms of depression in AD
5. **Atypical antipsychotics** for psychotic symptoms and agitation
77
other risk factors of PD
1. many blows to the head
2. stroke
3. tumor
4. brain infection
78
what are high plaque normals
those who have high plaque but don't show symptoms of Alzheimers
79
describe the role of microglia in Alzheimers
* help protect neurons early on by surrounding amyloid plaques and degrading them
* in later stages can trigger inflammatory state that leads to tau build up, dying of neurons, and cognitive decline
