1
Q
question: ventral vs dorsal streams? (where are they? what are they?)
A
VENTRAL
- what path
- from occipital to temporal
- conscious
DORSAL
- where path
- from occipital to parietal
- unconscious
2
Q
explain: patient DF (damage in ventral stream)
A
- visual form agnosia
⤷ cannot recog. objects visually
⤷ can recog. w/ other senses
3
Q
explain: patient VK (lesion in dorsal stream)
A
- can recog. things visually
- has difficulties scaling grasp when reaching for things
⤷ aiming hand when trying to pick things up
4
Q
define: traumatic brain injury (TBI)
A
- damage/injury to brain caused by external force/trauma
⤷ after birth
⤷ not hereditary, congenital, degenerative
5
Q
define + explain: open vs closed head injuries
A
OPEN
- penetration of the skull
CLOSED
- concussion
6
Q
define: coup + countercoup
A
- coup = site of a blow
- countercoup = second area of damage
**ex. brain can be damaged by compression on the side of the skull opposite to the coup
7
Q
question: what can happen as a result of severe coups/countercoups?
A
- bleeding
- subdural hematoma
⤷ bleeding under dura mater - concussion
8
Q
define: dementia pugilistica (causes?)
A
- boxer’s syndrome
- repeated mild head injuries
⤷ repetitive concussions - another name for chronic traumatic encephalopathy (CTE)
⤷ progressive, degenerative brain disease from repeated head trauma
9
Q
name: diff. names for CTE (6)
A
- dementia pugilistica
- traumatic encephalopathy
- chronic boxer’s encephalopathy
- chronic traumatic brain injury
- post-traumatic encephalopathy
- traumatic brain injury-induced neurodegeneration
**CTE = chronic traumatic encephalopathy
10
Q
question: is CTE limited on athletes?
A
- no
- can occur in anyone who has sufferent repeated head trauma
11
Q
explain: relation of P-tau to Boxer’s syndrome
A
- found in abnormal deposits of ppl w/ Boxer’s syndrome
- thought to contribute to brain cell degeneration + dev. of cognitive and behavioural symptoms of the condition
**P-tau is a key marker of CTE but other factors involved in developing the condition
12
Q
explain: function of P-tau
A
- phosphorylated Tau prot.
- attaching phosphate to prot. -> loses ability to move nutrients
- Tau helps stabilize microtubules
⤷ microtubules help transport nutriends
13
Q
question: what happens w/ the E4 variant of APOE?
A
- APOE = apolipoprotein gene
- E4 variant of the gene may have increased risk of developing brain injuries
- APOE helps move fats + repair brain from injury
**variant does not guarantee injury, but suggests increased vulnerability
14
Q
name: symptoms of Boxer’s syndrome
A
- progressive declining cognitive ability
- short term memory loss
- tremors
- loss of coordination
- difficult in speech
- changes in gait
- emotional disturbances
15
Q
question: do you need to hit your head to get a concussion?
A
- no
- can be a blow to head/neck/etc., whiplash
16
Q
question: is prolonged “brain rest” necessary after a concussion?
A
- no
- sitting around thinking about symptoms can make it worse
⤷ can take on a sick role psychologically - try to go about daily life after a few days of rest
⤷ until symptoms show up, then stop
17
Q
define: concussion
A
- closed head injury that can affect the way a person may think/remember things
- appear to affect healthy neural signaling
⤷ impact the axon of neurons
18
Q
question: how does mental health impact recovery after a concussion?
A
- difficult to predict which patients will struggle w/ lengthy recovery
- post-injury anxiety is an important factor
⤷ anxiety both before and after = linked w/ higher risk
19
Q
question: concussion rates in males vs females? age range?
A
- higher in males vs females
- higher risk from ages 10 - 29
20
Q
name + explain: types of tumours (2)
A
- malignant
- lack distinct boundaries
⤷ can spread
- likely to recur following surgical removal - benign
- contained w/in it’s own membrane
- easier to remove surgically
21
Q
define: metastasis
A
- malignant tumours shedding cells + travelling to other sites
22
Q
explain: meningioma
A
- tumour that grows out of the meninges
⤷ protect outer layers of the brain - usually benign
- easy to remove
⤷ bc close to brain surface
23
Q
define: glioma
A
- tumour developing in glial cells
24
Q
name: symptoms of tumours
A
- psi in skull
- specific disruptions related to location
25
name + explain: grades of tumours
I = benign, slow growing, respond well to surgery
II = malignant, slow growing, increased likelihood of recurrence
III = malignant, increased likelihood of recurrence, req. aggressive treatment
IV = rapidly fatal
26
name + explain: types of treatment for tumours (4)
1. **surgery**
2. **radiation therapy**
- high E radiation to target + destroy cancer cells
- can be internally or externally
3. **chemotherapy**
- administration of medication
- targets rapidly dividing cells
4. **targeted therapy**
- like chemo., but more specific to cancer cells
⤷ limited damage to normal cells
- disrupts signaling pathways/mech. that support cancer cell growth and division
27
define: MS
- multiple sclerosis
- chronic autoimmune disease
- affects CNS (brain + spinal cord)
- immune system mistakenly attacks myelin (oligodendrocytes)
⤷ causes inflammation, damage, disruption to nerve signals
- characterized by scar tissue in white matter of CNS
28
question: when does MS first appear?
- young adulthood
- ages 20 - 40
29
question: is MS more common in biological females or males?
- 2x more common in female assigned at birth
**modest heritability + envrt. factors
30
name + explain: factors explaining why MS affects males vs females diff. (4)
1. **hormonal factors**
- estrogen can affect immune sys. (can increase risk)
2. **genetic factors**
- genetic variations can increase risk for females
3. **immune sys. diff.**
- immune sys. of women can be more susceptible than males
4. **vitamin D**
- low lvls of vitamin D = linked to increased MS risk
- females more likely to have low vitamin D
31
name: symptoms of MS
- numbness
- tingling
- pain
- fatigue
- muscle spasms
- walking difficulty
32
define: AIDS
- acquired immune deficiency syndrome
- can lead to many neurological symptoms as a result of having HIV
⤷ human immunodeficiency virus
33
question: AIDS vs HIV?
- a person can have HIV but not have the status of AIDS
⤷ need enough decrease in WBC
⤷ need enough of the virus
**aka AIDS = more advanced stage of HIV
34
name: initial vs advanced symptoms of AIDS
INITIAL
- difficulty concentrating
- forgetfulness
- apathy
- musc. weakness
- social withdrawal
- decreased productivity
ADVANCED
- motor + cog. disturbances
**initial symptoms often misdiagnosed as (pseudo)depression
35
explain: 90-90-90
- 90-90-90 targets for HIV by 2020
- wanted:
⤷ 90% of HIV patients to be diagnosed (increase education about diagnosis and recognition)
⤷ 90% of diagnosed patients to get treatment (managing HIV)
⤷ 90% of patients on treatment to achieve viral suppression (prevent progression to AIDS, "cure" HIV)
36
question: what does HIV attack?
- indirect attacks
⤷ affects through impact on WBC
- invades:
⤷ **macrophages** = WBC that destroys harmful bac + waste
⤷ **microglia** = macrophages of the CNS
⤷ **astrocytes** = glial (support) cells that give structural support to neurons (hold them in place)
⤷ **vascular endothelial cells** = layer the blood vessels to support blood flow (carries nutrients)
37
question: how does HIV attack? (what mechanism? on a cellular lvl)
- infect cells release cytokines -> cause damage + apoptosis
⤷ cytokines = chemical messengers important in immune sys.
- too many cytokines can be bad
⤷ can apoptosis -> cell becomes non func.
- HIV can also bind to specialized prot. struc. -> excessive Ca+ -> neuron death
(3.2) psych 2nf3
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