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PSYC 301 MT2 > Causes of brain dysfunction > Flashcards

Causes of brain dysfunction Flashcards

1
Q

Meningiomas

A
  • tumours (neoplasms)
  • grow between the meninges
  • most common benign tumour
  • not very aggressive in growth
  • if you get rid, likely won’t come back
  • encapsulated (boundary btw tumour and rest of tissue) therefore easier to remove
    than infiltrating
  • 20% of brain tumours
  • solution: open head surgery
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2
Q

infiltrating tumours

A
  • malignant- more aggressive, faster growing
  • grow diffusely through surrounding brain tissue
  • not necessarily metastatic (spreads) but no clear delineation of where tumour begins and ends
  • removal process usually also involved healthy tissue
  • usually short amount of time to live
  • more common
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3
Q

metastatic tumours

A
  • some infiltrating brain tumours grow from tumour fragments carried to the brain from another body part via bloodstream
  • commonly originates from breast or lung cancer
  • very aggressive
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4
Q

glioblastoma/ glioma

A
  • most common type of malignant brain tumour in adults
  • very aggressive, short survival rate (12-15 months after diagnosis)
  • 40% of all brain tumours
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5
Q

STROKE

A

sudden-onset cerebrovascular disorders that cause brain damage
- 2nd leading cause of death in world
common consequence: trouble speaking, coordination, confusion, disorientation, unilateral problems

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6
Q

infarct

A
  • central location of stroke
  • area of dead/dying tissue
  • doctor isn’t interested in infarct bc dies so quickly, concerned with penumbra
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7
Q

penumbra

A

dysfunctional area surrounding the infarct

  • doctor’s concern is this
  • sometimes this tissue dies, not always
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8
Q

ischemic stroke

A
  • clot blocks blood flow to area of brain
  • extent of damage depends where is blocked
  • larger clot predicts larger loss of function
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9
Q

hemorrhagic stroke

A
  • blood flowing freely out of broken artery
  • issue = fluid pressure on soft tissue, blood is toxic
  • more dangerous
  • spreads
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10
Q

aneurysm

A
  • cerebral hemorrhage
  • can be congenital or develop later
  • commonly base of brain (circle of Willis)
  • risk factors: diabetes, hypertension, smoking cigs, alc, aging
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11
Q

treatment options for aneurysm

A
  1. Clipping
    - requires craniotomy, lower rate of recurrence than option 2
    - reduces risk of rupture
    - pinch at neck with titanium clip
    - downside = open head surgery
    short term: greater risk, long term = better efficacy
  2. endovascular coiling: less invasive, higher rate of recurrence
    - travel through arteries (leg)
    - cathedra filled with platinum wire. platinum causes blood to clot (coagulation)

short term = less invasive
long term = higher rate recurrence

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12
Q

Cerebral ischemia

causes

A
  • disruption of blood supply to some area of brain.
  1. thrombosis: a plug
    - can be air bubble, fat, tumour,
    plug = thrombus
  2. embolism: moving thrombosis
  3. arteriosclerosis
    - narrowing of arteries
    - typically result of fat/cholesterol deposit
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13
Q

properties of cerebral ischemia

A
  1. takes while to develop (days)
    - damage more likely in some parts (i.e. HPC)
    - mechanisms vary btw brain structures
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14
Q

excitotoxicity

A

mechanism of ischemia-induced damage

  • excessive glu release
  • hard time maintaining resting membrane potential because oxygen/glucose aren’t getting to the neuron, which it needs to function (na-k pump)
  • under quiet conditions, Mg2+ blocks NMDA receptors but as membrane is depolarized, Mg2+ is pushed out of cell and NMDA receptor works. under these oxygen depleted conditions, it happens excessively
  • NMDA is permeable to Na and Ca (potent, triggers apoptosis in such high levels)
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15
Q

how to save penumbra

A

NMDA receptor agonists

- unfortunately doesn’t work too well. Block things that Ca signals to= cutting edge therapies for stroke

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16
Q

open-head injuries

A
  • usually very severe
  • high risk of infection, complications
  • high velocity is worse

penetrating (through skull into brain) or
perforating (comes out other side)

-mortality = 92% (73 at the scene)

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17
Q

radial wound

A

wound travels in skull, causes lacerations

- therefore lower velocity impact is better

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18
Q

closed-head injury/contusion

A
  • damage to cerebral circulatory system, producing internal hemorrhaging and a hematoma (solid swelling of clotted blood within the tissues)

contusion= bruise

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19
Q

types of hematoma

A

epidural: pressure on brain, not blood in brain
subdural: “”
intracranial: hemorrhage in brain

20
Q

coup contrecoup injury

A

coup =place where you hit
contrecoup = due to head jostling

  • contusions are usually coup contrecoup
21
Q

Mild traumatic brain injury

A
  • blow to head, no evidence of contusion or structural damage
  • synonymous with concussion
    but you can injure brain without concussion (subconcussive mtbi)
22
Q

concussion

A

its a syndrome
collection of symptoms (dizziness, nausea, headaches, focus, irritability)
- successive concussions = danger
- need 9-18 months to recover from 1

23
Q

chronic traumatic encephalopathy (CTE)

A

(aka dementia pugilistica, punch-drunk syndrome)

  • progressive, irreversible NGD
  • caused by repeated blows to head
  • loss of tissue in brain
  • can see evidence in 20s/30s
  • not just pro athletes, not just concussion (common in epilepsy, ASD if you bang head repeatedly, domestic abuse)
24
Q

tau & neurofibrillary tangles in CTE

A

Tau stabilizes cytoskeleton

  • in CTE, tau gets hyperphosphorylated, causing it to bind to self instead of cytoskeleton, then cytoskeleton collapses
  • tau aggregates = neurofibrillary tangles
  • could be cause or effect on CTE (only looked at in most mortem)
  • also seen in AD, PD
25
Q

tau progression

A
  • different in CTE than AD
  • in CTE, see changes first in sulci of cortex
  • in AD, seen in temporal cortex and frontal first
26
Q

taupathy

A

class of neurodegenerative diseases (AD, PD, CTE) associated with the pathological aggregation of tau protein (neurofibrillary tangles)

  • trying to develop PET tracer for CTE diagnosis in living
    problem: tracer isn’t good enough yet, doesn’t bind across brain
27
Q

bacterial infections

A
  • bacteria attack brain, lead to formation of cerebral abscesses (pus pockets)
  • bacteria = living cell. bigger than virus. enters brain through blood stream
28
Q

Meningitis

A

inflammation in meninges

  • viral and bacterial
  • bacterial is more fatal/dangerous- fatal in 25% of cases
  • can’t know which one it is in the moment
    symptoms: fatigue, fever, confusion, irritability, light sensitivity

viral: few strategies
- best thing is to take care of secondary issues (staying hydrated)

29
Q

Syphilis

A
  • bacteria that can attack brain
  • takes long time before harmful
  • cured by one round of antibiotics, easy to test for
  • dormant stage: 15-20 years sometimes, easy to assess with skin test, no symptoms
  • then you get hallucinations, delusions, general paresis
30
Q

general paresis

A
  • loss of touch with reality

- psychosis/dementia that results from syphilis

31
Q

2 types of viral infections

A
  1. those that have a particular affinity for neural tissue

2. those that attack all tissue indiscriminately, including nervous tissue

32
Q

virus

A
  • clump of protein

- uses our genetic machinery to reproduce new versions of itself

33
Q

Rabies

A
  • affinity for NS
  • when bit by rabid animal, 15% chance of development
  • reciprocal nature btw symptoms and transmission (common symptom = aggression which makes more likely to bite)
  • travels to brain through motor axons retrograde
  • takes about 1 month to spread
    symptoms: unhappy, headache, fever, acute pain, excitement, trouble swallowing (hydrophobia). low energy, then mani, then coma, then death
  • fatal part is respiratory depression
34
Q

toxoplasma gondii

A
  • eukaryotic parasite
  • single cell bacterium
  • life cycle it requires it to be in and out of cat
  • goes out through feces/urine, rodent comes in contact with it. parasite gets into rat CNS and targets amygdala circuit that make rats afraid of cat scent. rats are now not afraid of cat (attracted maybe even) and cat kills and eats. life cycle repeats
  • high rates in humans (25-33% of cat owners), so far small beh. differences (higher on schiz. measures)
35
Q

neurocysticercosis

A
  • tape worm in brain
  • parasite infection
  • from contaminated food
  • at specific part of life cycle it can get into CNS and soft tissue inc. skin
  • form cysts= loss of function similar to tumours
36
Q

mercury exposure

A
  • can lead to toxic psychosis= hallucinations, delusions,
  • accumulates in brain, permanent damage
  • inhaling is most dangerous “mad hatter”- ppl who made hats breathed it in
37
Q

where is mercury

A

teeth fillings
vaccines- ethyl. but no evidence to suggest harmful effects
diet- methyl in fish

38
Q

minimata disease

A
  • caused by severe methylmercury poisoning
  • ataxia (lack of voluntary coordination of muscle movements), numbness, muscle weakness, damage to vision/hearing/speech, paralysis, coma, death, cogenital (present from birth) effects
39
Q

lead exposure

A
  • can lead to toxic psychosis
  • no safe exposure limit
    Flint Michigan: city with lead contamination in water
  • “crackpots”- tea pots from Victorian era made of lead. Cracked = die
40
Q

MS

A

progressive disorder that attacks myelin of axons in CNS, also cell loss. immune system attacks myelin as if it were foreign

41
Q

symptoms of MS

A
  • visual disturbances
  • muscle weakness
  • loss of motor coordination
  • tremors (we all have underlying tremor, but our muscle tone holds us rigid. When you remove this muscle tone, you see tremor)
42
Q

2 forms MS

A
  1. Relapsing-remitting: in yours 20s, weird couple of days. then it disappears, comes back a few years later. period with and without symptoms. period with symptoms gets more and more across lifetime
  2. Primary progressive: gradual appearance of symptoms. usually later in life
43
Q

theories of MS-pathogenesis

A
  1. primarily an autoimmune disease (outside-in theory)

2. primarily a NDG with inflammation in some patients (inside out theory)

44
Q

evidence for inside-out theory

A

(NDG)

  1. earliest problem appear to be on innermost layers of myelin (close to axon)
  2. in many patients, abnormal patterns of white matter is seen “bright spots”-glial scarring. Many patients don’t show markers of immune response
  3. often use an immune modulator to help MS- effective at getting rid of symptoms in relapse-remitting period, yet progression does not change
45
Q

what part of world has higher incidents of MS? Why?

A

Northern states. Canada

Culprit: exposure to sun/UV rays

Vitamin D promotes calcium absorption in gut. exposure to vit d is important in first 15 years of lie. lack of it is risk factor for MS

correlation between ppl who take vitamin d have lower incidence of MS later on

  • also genetics: ppl of European descent at a higher risk
46
Q

Treatments for MS? (8)

A
  1. Vitamin D supplements - potential to reduce risk, don’t help once developed
  2. Corticosteroids*- harmful side effects
  3. Immune system modulators* (good at relieving symptoms during r-r but won’t stop progression)
  4. Cannabis (Sativex)- reduce muscle rigidity
  5. P.T.- when symptoms are manageable
  6. muscle relaxants- reduce muscle rigidity
  7. Liberation treatment of veins- NO!
  8. High dose biotin- still in trial

PSYC 301 MT2 (5 decks)

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