Final Flashcards
(123 cards)
1
Q
State the 4 common themes of defining consciousness
A
Being Awake
Having internal subjective experience
Oriented to a moment in time and space
able to respond to things around you
2
Q
State the characteristics of a Coma
A
non awake, non aware, non behaving .
3
Q
State the Four different conscious states
A
Coma, Unresponsive wakefulness syndrome, Cognitive Motor Dissociation, Minimally conscious state
Coma, UWS, CMD, MCS
4
Q
Coma stereotype responses to pain
A
Decorticate posturing
- indicated higher level brain injury
- curled wrists, balled hands against chest, arms bent toward center of body
Decerebrate posturing
- indicate lower level brain injury
- straight, tense arms parallel to body, curled fingers, flexed wrists
5
Q
Key component of the causes of a Coma
A
Disfacilitation.
when there are very few action potentials fired
positive potassium ions leak out of the cells
resting membrane potential drifts negatively
Cell HYPERPOLARISES
in the cortex and striatum
6
Q
Describe the functional changes in the Brain from a coma
A
Theres a functional disconnection in the arousal network in the brain, structures are not acting together like normal
7
Q
What is Unresponsive Wakefulness Syndrome
A
Arousal without awareness.
Sleep-wake cycles intact, but not evidence of awareness of the environment around them
shows some reflexive behaviors
8
Q
What is Cognitive Motor Dissociation CMD
A
Awake with a little bit of awareness but presents the same as UWS. Covert consciousness!
Found using EEG and fMRI
CMD status predicted patient functional recovery at 1 year
9
Q
What is Minimally Conscious state
A
Patient is wakeful and shows minimal but inconsistent awareness
- some behaviour not attributable to reflexes, localisation of pain
sometimes language
10
Q
What are the components of the Glasgow coma scale
A
Eyes, (open to stimulus)
verbal, (answer question/make sounds)
and motor skills (obey commands/ abnormal flexion (posturing responses))
Entire scale out of 15, minimum score is 3
11
Q
Prognostication for DoCs (UWS)
A
UWS: 66-90% will improve consciousness but only to MCS
80% of UWS with CMD improve consciousness the remaining without only have 20% chance
1/5 chance that people who achieve MCS within 6mo will regain functional independence in the home
12
Q
Treatment of Disorders of Consciousness
A
Amantadine–> stimulant that promotes dopamine signaling
others:
- drugs for inflammation
- deep brain stimulation of thalamus
- repeated TMR
13
Q
Comment on socioemotional changes related to aging
A
People have smaller but more emotionally close social networks
greater emotional stability and complexity
cognitive decline in long term and working memory
processing speed declines
14
Q
Name and describe 4 physical changes affecting the aging brain
A
Volume loss: shrinks by 5% per decade after 40
- begins in frontal cortex, decline in basal ganglia and temporal lobe
Neurotransmitter depletion (dopamine and serotonin level decline)
Decreased Cerebral blood flow
Accumulation of damage to white matter linked to blood pressure
15
Q
Difference between normal aging, MCI and AD
A
Normal aging: decline in LTM and working memory
- processing speed decline
MCI: changes in attention and memory serious enough to be noticed by the person/friends/family
in excess of normal aging but activities of daily life preserved
Alzheimer’s disease/ dementia: impairment of multiple cognitive functions that affects daily living
16
Q
Prognosis of Mild Cognitive impairment
A
12-20% of people above 65 receive this
5-15% receive diagnosis of dementia that year
its sometimes a prodrome to Alzheimer’s but not always
17
Q
What is dementia
A
impairment of multiple cognitive functions that affect daily living
associated with progressive decline
onset in middle-to late adulthood
18
Q
Causes of Dementia
A
Alzheimer’s is the most common
Others exist too: Huntington’s, alcohol related etc.
19
Q
Describe early and later symptoms of Alzheimer’s
A
Early: confusion, irritability, deterioration of speech
Later: difficulties with simple behaviors/responses
- swallowing/ Speech
CAN ONLY fully DIAGNOSE ALZHEIMERS WHEN THEY ARE DEAED BY OBSERVING BRAIN TISSUE
20
Q
predictors of progression from MCI to AD
A
Older age
Genetic status Apo-E epsilon 4
medial temporal lobe atrophy on MRI
Dysfunction in amyloid and tau
biomarkers in cerebrospinal fluid
21
Q
Clinical Significance of Apo-E status
A
Everyone carries 2 Apo-E proteins (either 2,3,4)
BUT the more of their 2 copies is ApoE4, the more likely it is that they get alzheimers
- homozygous for 4 predicts frequency of 91%
22
Q
List the defining characteristics of Alzheimer’s
A
- Neurofibrillary tangles
- Amyloid Plaques
- Volume loss
23
Q
what are neurofibrillary tangles
A
Tauopathy: tau proteins misfold and build up
- extra phosphate group added to the tau that causes them to misfold
cell loses its structure and these misfolded proteins build up INSIDE THE CELL
misfolded tau proteins cause all the other ones to misfold too
24
Q
Describe amyloid plaques
A
amyloid proteins take on large collapsed forms in healthy aging over time but this is cleared using normal mechanisms.
In Alzheimer’s, the collapsed forms build up and become too much for the body to clear and handle
a pathological buildup OUTSIDE THE CELLS
25
describe volume loss as a cause of Alzheimer's
the progressive loss of total number of cells and synapses between cells
appears first in medial temporal lobes
probably driven by tauopathies and amyloid plaques
26
How does the progression of pathology for Alzheimer's unfold over time
first amyloid beta plaques form
then there tauopathy
then volume loss
changes in cognitive come after
then changes in person's life
27
List the two theories for AD
Amyloid Cascade Hypothesis
Neurofibrillary tau hypothesis
28
What is the Amyloid Cascade hypothesis + evidence+ issues
The dominant theory for Alzheimer's
says that amyloid plaques are the primary symptom that causes all the other damage
evidence : from people with **down syndrome since they have copies of chromosome 21 ( the gene for amyloid)
100% of them develop amyloid plaques during aging
BUT there exist people who normally have high amyloid plaque who don't have AD
Amyloid drugs don't really work
29
What is Neurofibrillary tau hypothesis + evidence
Another theory for the cause of Alzheimer's
basically says that misfolded tau is the causal agent
evidence: tau pathology correlated better with cognitive impairment compared to Amyloid
30
Treatments for Alzheimer's
They all focus on management more than curing
Cholinergic agonists
- prevent breakdown of ACh, prevents decline in learning and memory
NMDA receptor agonists
- slows down damage to neurons
Target modifiable risk factors
- depression, smoking, social isolation
31
What are Biomarkers
The test of Alzheimer's
Markers in the cerebrospinal fluid that are related to amyloid and tau
informs diagnosis, treatment and referral
results need to informed responsibly
32
What are the motivating factors to classify mental illness
To seek similarities and differences among patient groups
- guide treatment choices
- create a common language for clinicials etc. to communicate
- for those who need diagnosis (insurance, CFA etc.)
- to permit research
33
List the three traits of the DSM's approach
Atheoretical
operationalist
categorical (black and white diagnosis)
34
List some criticisms of the DSM
Heterogeneity of criteria
(unevenness across different diagnoses)
problem of overlap
2 people can have no symptoms in common but same diagnosis
2 people can have same symptoms but different diagnoses (overlap of symptoms)
Authority for symptoms varies
sometimes its clinician judgment, other times its the patient
Comparators
some compare to the self, other times its normative statements etc.
35
Define normative assumptions + trends
Diagnosis contains evaluation of what is right and wrong, based on societal beliefs
as opposed to descriptive statements
(masturbation, Homosexuality)
36
Define deinstitutionalization + trends
The concept of how people are MI are treated and living within the community.
1960s, movement that moved ppl out of institutions, many ended up incarcerated
They need adequate support within the social system to not get institutionalized
37
Comment on mental illness and violence
People with MI are not more violent than others from same neighborhoods
- MI alone is not a predictor of violent behaviour
- Violence associated with poverty, discrimination, structural inequality
38
List the DSM criteria for schizophrenia
at least 2 of:
- delusions
- hallucination
- disorganized speech
- catatonia
- negative symptoms
Functioning is below level prior to onset (causing distress/disturbance)
Continuous signs of disturbance persist for 6 months
other disorders/ substances ruled out
39
List the 3 symptom categories for schizophrenia
Positive symptoms
Negative symptoms
cognitive symptoms
40
What are positive symptoms of schizophrenia
New mental phenomena that don't occur normally
hallucination and delusions
41
What are negative symptoms of schizophrenia
Flattened affect
Impoverished content of thought and speech
lower social motivation
42
What the cognitive abnormalities symptoms of schizophrenia
impaired working memory
impaired executive function
Impaired source monitoring (can't tell if they imagined smth or did it)
Schizophrenic speech
43
Prevalence of schizophrenia
0.5-1% have it
slightly more common in men
preceded by prodromal period
44
Risk factors of schizophrenia (5)
Genetics
Urban environment
events in pregnancy (1st and 2nd trimester)
use of cannabis or stimulants
bio father is over 35 at conception
45
Common structural brain changes in schizophrenics
Decreased pattern of grey matter
thinning of dLPFC
less total brain matter in the skull
reduction in cell processes (fewer axons and dendrites)
fewer GABAergic inhibitory interneurons
Hippocampus structural changes, disorganised layers
46
Functional brain changes in schizophrenia
Hypoactivity in frontal and temporal lobes
and in hippocampus
show less dLPFC activity when doing working memory tasks
47
Treatments and side effects of schizophrenia
Antipsychotics
typical: chlorpromazine, haloperidol
act on dopamine (can lead to Parkinson's like movement disorders)
Atypical: olanzapine, aripiprazole
act on dopamine, serotonin etc.
metabolic side effects
all treat positive symptoms mostly
48
List the 2 theories of schizophrenia
Dopamine theory
Glutamate hypofunction theory
49
What is the dopamine theory of schizophrenia
schizophrenia caused by too much activity at dopamine receptors
Evidence: antipsychotics produce symptoms similar to Parkinson's disease (parkinsons is caused by dopamine depletions)
- drugs that increase dopamine (cocaine, amphetamine) can produce symptoms of schizophrenia
-
50
Issues with the dopamine theory of schizophrenia
newer drugs don't just target dopamine and are just as good as older antipsychotics at treating positive symptoms
takes 2-3weeks for antipsychotics to work even though their effects on dopamine are immediate
Most patients show not improvement to the first antipsychotic drug they try
51
Describe the Glutamate Hypofunction theory of schizophrenia
Ketamine and PCP induce the negative and positive symptoms of schizophrenia
- these act on the glutamate system
-----------------------------
The glutamate neuron is excitatory. when it binds on a postsynaptic cell, it excites them
Glutamate neurons often synapses onto GABAergic neuron
-glutamate binds to NMDA receptors that let through calcium that leads to changes in post-synaptic cell
- When GABA neuron act in inhibitory ways on the rest of brain
--------------------------------
In schizophrenia, there's abnormal glutamate signaling,
= less GABAergic transmission (less inhibition)
so too much activity/ excitation in the rest of the brain
52
What is eythymia
the normal band for mood swings
53
state DSM criteria for hypomania
persistent, elevated, expansive or irritable mood
increased goal-directed activity or energy most of the time for at least 4 days
- increased acitivty/energy
- mild elevation of mood
- increased social, sexual energy
- decreased need for sleep
BUT none to the extent that they have severe disruption of work/ social life
AND no hallucination/delusions
54
DSM 5 criteria for Manic Episode
Hypomanic symptoms last at least a week
inflated self-esteem
experience that thoughts are racing
excessive involvement in high risk activities
AND marked impairment in social/work life, necessitates hospitalization or includes psychosis
55
Difference between Bipolar I and II
Bipolar I= depression + mania
Bipolar II= depression + hypomania
56
What is the reward hypersensitivity model of BD
A mechanism that explains the cycling of mood.
Hypersensitivity to reward predisposes someone to developing BD
- goal attainment leads to excessive reward states (hypomania)
goal nonattainment leads to reward deactivation
(depression)
57
Evidence for the reward hypersensitivity model(3)
1. euthymic individuals with BD show excessive activity in reward related areas in response to reward related cues (money sign when gambling
2. prodromal features
Hypomania/mania has excessive goal setting and higher success expectancies
depression episodes has decreased motivation and goal setting
3. teens who score higher on reward sensitivity more likely to develop bipolar disorder
58
List the functional brain changes in euthymic BD patients
higher responsiveness in LIMBIC and PARALIMBIC areas
- amygdala, VLPFC, Ventral ACC
Decreased responsiveness in cognitive control areas
- Dorsal ACC
- DMPFC
-DLPFC
59
Structural changes in BD patients
reductions in grey matter
- associated with time spent in manic states
- due to inflammation and stress hormones
60
List the treatments of BD
Lithium! Mood stabilizers.
Psychotherapy --> CBT, health education
not antidepressants alone! because they can push someone into elevated mood state
61
Challenges to treating BD
Not all patients adhere to medications because their mood is always changing
- less than 50% ahdere to treatment
62
State the prevalence of Bipolar Disorder
0.6 for BD one
0.4 for BD two
Steep rise in diagnoses in teens and 20s
63
Name the three components of executive function
Holding and working with information mentally
Resisting temptation (inhibitory control)
Cognitive flexibility (being able to change perspective/ tasks)
64
List the test for working memory
digit/ pointing span
65
test for inhibitory control
stroop colour word task
Flanker task
66
Test for cognitive flexibility
Wisconsin card sort
trail making with alternation
67
how does the mental status exam test executive function
judgment tests
verbal fluency tests
luria's 3 step test (fist,edge,palm)
trail making
clock drawing
68
the three consequences of frontal lobe damage
Abulia - lack of drive
Utilization behaviour- failure to inhibit automatic response
return of primitive reflexes - movement present
early on that are inhibited in adulthood come back (infant reflexes)
69
Two relevant parts of the PFC in executive function
Orbitofrontal circuit (lower on both sides of PFC)
Dorsolateral circuit (Higher, frontal side of PFC)
70
Effect of damage to orbitofrontal circuit
Impulsive, socially inappropriate behaviour
- poor safety judgment
- difficulty evaluating anticipated reward/punishment
- don't learn from mistakes in the past
71
Effect of dorsolateral circuit damage
distractibility, disorganized, difficulty multitasking
poor time management and prioritization
72
major symptoms of ADHD
Extreme inattention, hyperactivity, impulsivity
73
prevalence of ADHD
5-7% of children (younger kids in classroom more likely- shows environmental factor)
2-3% of adults
74
Describe the neurobiology of ADHD
Lower activity and volume of PFC
- less activity in orbitofrontal cortex (part of the PFC)
Normal people: PFC starts thicker and thins
ADHD ppl: PFC starts thinner but doesn't thin out as much
- thinness of the PFC correlated with the symptoms
75
what is the dual pathway model of ADHD
ADHD involved the DLPFC and the caudate
- there's also parallel dysfunction of reward circuitry (in orbitofrontal cortex, anterior-cingulate and nucleus acumens)
76
List the 3 types of ADHD
ADHD-I, (inattentive)
trouble focusing, disorganization
ADHD-HI (Hyperactive impulsive)
Disruptive, fidgeting etc.
Combination
77
Treatment of ADHD
Mediations that act on dopamine and norepinephrine systems in PFC and subcortical structures
(because theres evidence of a hypoactive dopamine system in ADHD)
78
Define Stigma
A sign of social unacceptability,
negative attitudes, beliefs, behaviour toward an individual or group based on a commonality they're perceived to share
79
types of stigma
Public stigma
Systemic stigma
Self-stigma
80
Gender differences in ADHD diagnosis
In childhood: boys 3x more likely than girls to be diagnosed
Ratio become 1;1 in adulthood
81
Differential prevalence in ADHD subtype diagnosis
ADHD HI more likely to be diagnosed because its more disruptive and visible
82
Factors contributing to under/misdiagnosis of ADHD in women
Overrepresentation of boys in ADHD research
- diagnostic criteria geared toward male presentation of ADHD
- Women have greater presence of Comorbid disorders (bc of masking)
Higher threshold for symptom severity for women
83
Why is ADHD likely to be stigmatized
highly visible
perceived as controllable
misunderstood
84
2 types of self responding
its on a spectrum from:
Uncompassionate self-responding
(judgment and criticism)
Compassionate self-responding
(self-kindness and understanding)
85
three elements of self compassion
1. emotional response to our suffering
(kindness vs judgment)
2. how we cognitively understand our suffering
(common humanity vs isolation)
3: how we pay attention to our suffering
(mindfulness vs over-identifying with negative feelings)
86
Benefits of self-compassion for ADHD individuals
improved psychosocial wellbeing/ emotional regulation
better resilience, self-efficacy
reduced co-morbid symptoms and stress
87
Define Neuroplasticity
Experience-dependent change
the brain's capacity to change following experience
88
how many neurons does the brain have and how are they organised
80 million, organised in either 'rich club' or 'poor club'
89
What what Donald Hebb's famous finding
Neurons that fire together wire together
- neurons activated at the same time will strengthen their connection.
This produces networks that underlie all learning and memory
90
List the three mechanisms of neuroplasticity
Functional plasticity
Structural plasticity
Neurogenesis
91
What is functional plasticity (examples)
Strengthening or weakening of synapses based on experience
Long term potentiation= strengthening
Long term depression = weakening
Changes in gene expression/protein synthesis
Reorganization of firing patterns
92
What is structural plasticity (examples)
changes in the densities of cells
- dendrites and axons sprout new spines
regulation of synaptic pruning as a result of experiences
93
What is neurogenesis
the birth of new neurons from stem cells
not sure if this happens in human adults though
94
How is age-dependent plasticity demonstrated in rats
When rats are put into condos from shoeboxes in infancy, they had a decrease in spine density in the cortex
when changed environments in adulthood, they found increase in spine density in the cortex
95
Age dependent plasticity demonstrated in humans
Children born with cataracts
Have more plasticity since they develop amblyopia that remained even after the cataracts were removed
Adults: did not develop amblyopia and won't show deficits once the cataract is removed
ALSO children born without vision, V1 takes on other functions: sound, language, touch - demonstrates plastic changes
96
What is Charles bonnet syndrome
Phantom vision
Adults who go blind report visual phenomena because V1 starts firing spontaneously
97
How can cortical maps help us measure plasticity
Somatosensory and motor homunculi gives us an index of plasticity by mapping how much of the cortex is devoted to specific parts of the body
Study used TMS and EEG to map how much of the cortex is devoted to specific fingers
- there was enlargement of right finger cortical tissue in people who read braille compared to people who don't (they had even distribution)
98
What is focal dystonia + evidence
Disorder involving involuntary muscle movement and postures of an overused body part
Happens to musicians/ surgeons etc.
due to a change in the motor maps, they expand and overlap one another
Example of a PATHOLOGICAL PLASTICITY
Evidence: study on monkeys
overtrained in repetitive movements, finger maps got much larger
- found a change from the normal arrangement of the maps
99
how can interventions target neuroplasticity
can induce plasticity in the glutamate synapse
triggers NMDA and AMPA receptors to produce calcium signaling
Lead to production of BRAIN-DERIVED NEUROTROPHIC FACTOR BDNF
BDNF acts on the same cell that created it and changes the expression of glutamate receptors
100
List some interventions that change plasticity
psychedelics
Antidepressants
do this by making cells more receptive to BDNF
TMS and ECT does this too
101
Define neuropathic pain
pain caused by a lesion or disease of the somatosensory nervous system
102
causes and prevalence of neuropathic pain
causes: spinal cord injury, diabetic neuropathy, Cancer etc.
Affects 7-10% of population
103
Define central sensitization
A plastic change in pain processing in the CNS
104
State the three causes/ types of central sensitization
1. allodynia
- pain response to usually non-painful stimuli
- stroking sunburnt skin
2. primary hyperalgesia
- already painful sensations become more painful in the same location
- pelvic pain made worse by period
3. secondary hyperalgesia
- increased pain to painful stimuli in areas outside of original injury
- knee surgery leads to sensitive skin around the knee
105
List the mechanisms of central sensitization
Spontaneous activity in the spinal cord
- unbalanced pain and touch signals drive increased excitability and receptive field size of CNS
- damaged inhibitory circuits in brainstem and spinal cord (normal pain inhibition is lost)
106
Define cognitive rehabilitation therapy
therapy aimed to improve cognitive functioning through combined action of compensation, plasticity and recovery
- used for TBI and Stroke
107
The two parts of Cognitive rehabilitation therapy
Training affected behaviours (target plasticity+ compensation)
Offer external supports (target compensation)
108
list some areas where cognitive rehabilitation therapy has good evidence of working
attention deficits after TBI/Stroke
Visual scanning for neglect after right-hemisphere stroke
Mild memory deficits
109
What is the traditional extractive model of research
Treats patients like a source of data
- research team makes all the decision, determines research topic and method
interactions with ppts happen on researcher's terms
Results published in closed-access journals
110
Describe models of patients engagement in research
patients as long term advisors
collaboration with patients to develop the research
focus groups/interviews
patients involved as experts on the research methodology itself
111
List some barriers to the inclusion of people with lived experience (patients) in research
Resource-intensive
Researchers fear giving away power (patients might shift research agendas)
Lack of supportive infrastructure and research culture (no expertise on how to do this well)
Fear of tokensim (letting one person speak for everyone)
112
Arguments for patient engagement in research for the researcher
Ethical/moral argument (nothing about us without us)
Advantage for researchers (helps retention in studies, since the experience is better for patients)
Improves quality of research itself (better data collection tools, wording etc.)
Dissemination and mobilization of findings (circulates information in accessible way for patient users)
113
list a few positive outcomes for patients who engage in research
empowerment
feeling of value, confidence
better trust between researcher and patient
better quality of care
114
5 properties of big data
Volume
Variety
velocity (how quickly data is generated)
veracity (how accurate it is in terms of what its supposed to be doing)
value
115
Define AI
Artificial systems that appear to think like humans
decide, categorize, recognize
116
What is Machine learning
subset of AI, systems that can learn from expereince or data without direct human programming
117
list the 2 types of machine learning
supervised learning : there's a right answer
Unsupervised learning: learn from unlabeled
118
List some AI applications in Neuroscience (5)
Risk prediction: trained ML model on MRI data to predict AD status
Clinical decision making: ML used to categorise implanted electrodes as being near or fear from seizure site
Neurotechnology's: Model trained using monkeys implanted with electrodes to relate action with activity. Used in humans to control limb prosthesis
Diagnosis and Prognostication
Brain modelling: using rats brains
119
list the 2 ethical issues around using AI in neuroscience
accountability
duty to explain (ai processes are unexplainable (black box results) doctors can't answer questions about it)
120
4 components of a social robot
sensors
actuators (moves)
autonomous (processes)
social (capable of interaction)
121
list the 4 brain health applications of social robots
emotional support
monitoring: pain, fall monitoring
health: physical therapy, dispensing medication
Connecting: telepresence, reporting
122
Potential harms of social robots
Privacy and security
Responsibility
Deception (misleading users about its nature)
Stigma
attachment (should we encourage someone to form to a relationship with a robot)
123
Social determinants of health risk factors for cognitive decline and dementia
single
single household
employed
social isolation
middle vs higher education
