Causes

Question 1

What are meningiomas?

Answer 1

Tumors (neoplasms) that grow between meninges. Encapsulated: boundary is clear. benign.

Not aggressive.
Solution: remove with surgery.

If it was placing pressure on anywhere, that pressure should be relieved. tumor itself isn’t problematic per-say

Question 2

What are infiltrating tumours?

Answer 2

Grow diffusely through surrounding brain tissue
Malignant, aggressive, faster growing.

influtrating: no boundaries,

in order to remove, you must take healthy tissues

worse outcomes associated

Question 3

What are metastatic tumours?

Answer 3

Some infultrating brain tumours that have grown from tumor fragments carried to the brain via bloodstream. Originate from breast or a lung cancer usually.

Question 4

What is a glioblastoma?

Answer 4

most common malignant brain tumor (glioma)
Most malignant
Short survival rate

common, aggressive

famouse ppl: Gord Downie and Bob Moog

Question 5

What are strokes? What are the associated areas?

Answer 5

onset of cerebrovascular disorders that cause brain damage.

common issues: trouble speaking, coordination, talking, drooping side of the body. Some symptoms go awaay

Infarct: area of dead/dying tissue. epicenter of the problem

Penumbra: dysfunctional area around infarct (may recover or die). it is getting some blood, so membrane polarity is retained, but it is functioning less than optimally. doctor’s goal is to save this part of ur brain.

Question 6

What are the types of strokes?

Answer 6

Ischemic: cerebral ischemia, blockage in arteries, so blood doesnt reach till the ends of the arteries. - damage depends on where the blockage is. Larger clot - larger damage

Hemorrhagic: bleeding in the brain. BLood flowing freely (toxic to neurons) and placing fluid pressure on soft tissues (fire extinguisher on jello)
More dangerous then ischemic

Question 7

What is an aneurysm?

Answer 7

Balloon type growth on an artery. Narrowing/tapering at the part where it connects. Expands like a water balloon with blood with the potential to burst!!
Congenital or develop later.
in base of brain (circle of willis)
Risk factors: diabetes, hypertension, smoking, alcoholism, aging. Usually an artery, Two treatments:

1) Clipping, requries surgery but lower rate of recurrence. Clip it shut at the neck and leave it in there (titanium clip that isn’t magnetic)
Better efficacy LONG term

2) Endovascular coiling. Less invasive, but higher rate of recurrence.
Traveling up through femoral artery, through heart, to the brain up to artery at risk. inside there is a cathedar with wire, shove wire into the aneurism that is made of platinum which causes coagulation/blood clots so that it won’t fill the hole up anymore!!
- real time x rays used.

Question 8

What are the 3 main causes of Ischemia?

Answer 8

Distruption of blood to an area

1) Thrombosis: a plug, bubble of air, blocking flow of blood
2) Embolism: a moving thrombosis. Grew in a not dangerous place and moved to a smaller artery
3) Arteriosclerosis: narrowing of blood vessels themselves via cholesteral, fat deposits.

often a combo of these things and can build up over time

Question 9

What are the 3 important properties for cerebral ischemia?

Answer 9

1. it takes a while to develop (can be days)
   - need to find markers for this!
2. Damage is more likely in some places of brain (hippo)
   - cells are more active and require lots of 02 all the time which is why they are more sensitive to cutoff
3. Mechanisms for ischemia induced damage can vary between brain structures (excitotoxicity and apoptosis)

Question 10

What is exitotoxicity?

Answer 10

When you get excessive glutamate release, often when you have a hard time maintaining RMP, so you depolarize membrane getting lots of APs. Glutamate has many receptors (ampa and nmda)
Ampar are for when its quiet (nmdar binds when its quiet but doesn’t do anything because of mg2 blocking it) .
as you depolarize, mg2 is pushed away and you have NMDA activity.
NMDA lets in sodium but ALSO calcium - great for strenghtening synapses and important for memory.
NMDAr receptors are usually active in development when we need to “prune” cells, because it triggers apoptosis.

when you have a stroke: gluatamate release, and therefor calcium release tells these cells to self destruct.

unfortunately blocking these receptors doesn’t really work, calcium can get in other ways. we block things that calcium signals too (downstream of NMDA)
***

Question 11

What are open head injuries?

Answer 11

typically fatal. High risk of infection.
High velocity is worse than low velocity.
penetrating: enters thru skull into brain
perforating: comes out the other side.

Radial wounds: travels around and around head.

Question 12

What are closed head injuries?

Answer 12

Contusions (bruise) 
Damage to cerebral circulatory system, producing internal hemmorhaging and resulting in hematoma (brain slams against skull) 
1) epidural (within menigies)
2) Subdural (within meningies still) 
3) worst - intracranial

Coup contrecoup (backlash, bouncing bath and forth, jostling riccoshet)

Question 13

When does coup contrecoup happen?

Answer 13

When you hit something stationary.

Question 14

What is mTBI?

Answer 14

mild traumatic brain injury. Blow to the head with no evidence of structural damage.
Same as concussion (syndrome)
But you can injure your brain without getting a concussion (subconcussive mTBIs: repeated hits to the head with a cumulative effect, even if you never get a single concussion)

Successive concussions: multiple before 1st has healed

Question 15

What is CTE?

Answer 15

chronic traumatic encephalopathy.
- Dementia pugilistica (punch drunk syndrome)
- progressive, irreversible neurodegenerative disease caused by repeated blows to the head.
loss of tissue in the brain.
not just concussion or in professional athletes. (ppl with epilepsy, autism, victims of domestic abuse)

Question 16

What is a clear marker of CTE postmortem?

Answer 16

Tau and neurofibrillary tangles.
- tau stabilizes the cytoskeleton fixing it in place, and when it is hyperphosphoylated (gets extra groups added to it, it binds to ITSELF instead of cytosteleton/ it aggregates and cytoskeleton becomes unstable. (not CAUSE but correlated)
Seen in Alzheimers and parkinson’s too.
relies on after death staining.

Question 17

How does Tau progress?

Answer 17

Sulci first, buildup of iron deposits from hemmorhages. The progression is different in CTE and in AD

Question 18

How do we see Tau

Answer 18

since it is a protein, you can use PET to trace where it binds, (give radioactive molecule (FDDNP) and see binding of tau (hyperphosphorylated binding)

however this isn’t yet good enough to diagnose or do things.

Question 19

What is the difference between bacteria and viruses? How do they get into our brains?

Answer 19

Bacteria: living cells, their own entities
Viruses: self replicating using our own machinery

Both get into our brain through bloodstream, randomly pass BBB even with efforts to keep them out.
We know BBB is more porous in some areas and things could slip in here but it is mostly dumb luck.
If they get in = infection occurs

Question 20

What are some Bacterial infections?

Answer 20

Cerebral absecesses (pus pockets) 
Attack meningies (inflammation known as meningitis)
Syphilis

Question 21

What is Meningitis?

Answer 21

Inflammation of meningies. (can be bacterial- more fatal or virus. only assessed post mortum if you have it)

• fever
• fatigue
• confusion/disorientation
• tiredness
• sensitivity to light
• in kids its hard to diagnose

example: stupid dad who tried to help his kid ‘naturally’ showed persistent symtoms. tried cold blast and mustard seed, only called 911 when he was siezing, and then he died.
appealing viral meningitis so nothing would have helped anyways.

Question 22

What is syphilis

Answer 22

Bacteria that can affect the brain.

GENERAL PARESIS: syndrome of psychosis that results from syphilitic infection of the brain (long term untreated)

easy to test for it (partially on our skin, can treat with antibotics easily)
dormant and can take decades to show up. Common transmission is genital

Question 23

What are the two types of viral infections?

Answer 23

1. affinity for neural tissue
2. attack all tissues indiscriminately.

Viruses are clumbs of protiens with RNA that use our machinery to reproduce.
May be a bigger role player in psychiatric disorders than we thought initially.
We can pass dormant viruses onto other who will get symptoms

Question 24

What is rabies?

Answer 24

a viral infection with an affinity for the nervous system.
If a rapid animal bites you, you have a 15% chance of getting rabies.
TRAVELS RETROGRADE through motor neurons to brain.

Symptoms: make you more aggressive, and in turn, more likely to bite and spread the disease.

Is lethal but takes about a month to attack the brain.
Malaise, Pain, fevers, TROUBLE SWALLOWING, hydrophobia, kind of like meningitis.
Total mania, then lethargy, coma then die of respiratory issues.

Question 25

What is toxoplasma gondii?

Answer 25

Eukaryotic parasite (single cell). 
Uses power of attraction to trick rats into being cat food. 

Lives in cats, then excreted. If rats get it, there is a SPECIFIC MECHANISM that if it gets into the CNS, it damages the rat’s amygdala (fear related) that is scared of the smell of cats and can even make the smell attractive. This makes the rats want to go find cats and get eaten!!!!

Not damaging to cats or people who have it. Ppl rank higher on schizophrenic personality measures. (business school students had higher measures too lol )

Question 26

What is Neurocysticercosis?

Answer 26

Tape worm in the brain!
Usually in our guts, but if they get into our bodies at a certain point in their life cycle, it can get into nervous system. Form cysts and cause loss of function similar to tumours. Growth is alive and gross.

Can be mistaken for a tumour.
Symptoms are non specific, nothing comes back on a cat scan, but DOES come back from an MRI. (why is that?)

Question 27

What happens if mercury gets into your brain?

Answer 27

Mercury: accumulate and cause toxic psychosis. Toxic if INHALED (think mad hatters)

Liquid or hard mercury isn’t so bad. see it in teeth fillings and vaccines.

Minamata disease: caused by severe methyl mercury (like in fish) poisoning. (motor problems, cognitive issues, ataxia, numbness, paralysis, congenital, death)

Ethyl is what is in vaccines and stuff.

Danger is in cooking it/vaporizing it.

Question 28

Who is wakefeild?

Answer 28

started public panic about vacinnes causing autism because he didn’t account for a control group when critisizing a study.

Question 29

What happens if you get lead in your system?

Answer 29

SUPER BAD:
crackpots, toxic psychosis.
no safe exposure. 0 is the limit.

Flint Michigan: lead i water supply, knocks IQ off a person.
Lead is in paint of older homes, teapots (watch out for cracks!)

Question 30

What is MS?

Answer 30

Progressive Disorder that attacks myelin of axons in the CNS. (cell loss too)

Visual disturbances, tremor (possibly tremor is always there and MS lets it come out) trouble with sensory and motor signals.

Immune system appears to attack CNS myelin like its a foreign substance.

Types

1) relapsing remitting: in your 20s, have a few weird days , then its gone, but often reappears later on. eventually turnes into 2) secondary progressive.
3) Primary progressive: general progression, happens later in life, one day it appears, gets worse and never goes away.

Question 31

What the theories of pathogenesis for MS?

What are the reasons for the inside out theory?

Answer 31

1. Autoimmune disease (outside in theory)
2. Neurodegenerative disease (inside out theory).

we think nowadays that it is a neurodegenerative disorder (loss of cells) that LEADS to an immune response that attacks myelin.

Inside out theory:

1) starts on inside, earliest myelin is damaged first.
2) Abnormal white matter patterns in the brain (bright spots) indicating glial scarring. Don’t always show big immune response like in regular autoimmune diseases.
3) Immune modulators are good at getting rid of relapsing remitting MS, but progression of diease does not change, you still get secondary eventually.

Question 32

What is CIS?

Answer 32

Clinically isolated syndrome.

First time you’re symptomatic in RRMS

Question 33

How does RRMS progress?

Answer 33

You have a threshold of problem that you show symptoms at, as degeneration gets worse, you often cross that shreshold. When cytodegeneration kicks in and you have symptoms.

Question 34

Why does Canada have highest levels in the world?

What are the genetic factors?

Answer 34

northern states do too!
Indicating of VITIMIN D deficiency.
VD promotes calcium absorption in the gut, ppl with enough VD have lower MS instances, best in the 1st 15 years of you life.

Ethnic/cultural background: europena decent have higher risk

More risk if your twin has it than a distant relative.

Question 35

What are the ‘treatments’ for MS?

Answer 35

1. VD supplements (can reduce risk)
2. Corticosteroids (used in lots of diseases)
3. Immune system modulators (effective for RRMS, but don’t stop progression)
4. Cannabis (can’t stop progression but will release spacitcity and stiffening)
5. Muscle therapy: can be helpful
6. Muscle relaxants (same as Sativax)
7. Liberation (NOPE) losening constricted blood vessels in brain. No results.
8. High dose biotin (helpful in other disorders)