Causes of Brain Dysfunction (Part 1) Flashcards

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1
Q

2 types of tumours

A
  • encapsulated

- infiltrating

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2
Q

encapsulated tumours

A
  • Grow between meninges
  • “Meningiomas”
  • Benign tumours -> can be removed without removing other tissues
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3
Q

infiltrating tumours

A
  • Grow diffusely through surrounding brain tissue
  • Malignant tumours -> cannot be removed without removing other important tissues
  • Ex. Metastatic tumours: grow from tumour fragments carried into the brain from another body part via the bloodstream; commonly originate from a breast cancer or lung cancer
  • Glioblastoma/glioma: problem with white matter/glia; most type of malignant brain tumour in adults; aggressive – life expectancy 12-15 months post-diagnosis
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4
Q

strokes (and tissues affected)

A
  • Sudden-onset cerebrovascular disorders that cause brain damage
  • Infarct: area of dead/dying tissue (not worth treating)
  • Penumbra: dysfunctional area surrounding the infarct; tissue in that area may either recover or die (treatment is focused on this)
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5
Q

2 major types of strokes

A
  • resulting from cerebral hemorrhage

- resulting from cerebral ischemia

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6
Q

strokes: resulting from hemmorhage

A
  • More severe type of stroke
  • Driven by aneurysms
    • Aneurysm: Blood pressure creates bubble of blood that may burst, damaging tissue (circle of Willis is prone to this)
  • – If it does burst -> hemorrhagic stroke
  • – Treatment: clipping it off (more invasive, more effective), “coiling” using tube going through artery into brain (less invasive, less effective)
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7
Q

strokes: resulting from cerebral ischemia (what it is; 3 main causes)

A
  • Disruption of blood supply to some area of the brain
  • 3 main causes: (can occur simultaneously)
    • Thrombosis: some sort of plug (plaque, blood clot, etc.) preventing blood from flowing past it
    • Embolism: “thrombosis on wheels”; thrombosis starts moving through the body
    • Arteriosclerosis: narrowing of blood vessels (due to fat deposits, cholesterol, etc.)
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8
Q

strokes: resulting from cerebral ischemia (3 properties of its brain damage)

A
  • Takes a while to develop
  • Damage more likely in some parts of brain (ie. Neurons in hippocampus)
  • Mechanisms of ischemia-induced damage vary between brain structures
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9
Q

strokes: resulting from cerebral ischemia (types of ischemia-produced damage)

A
  • Contralateral neglect – damage post-ischemia leaves you with an inability to pay attention to the left side of things (ie. A picture of a cat)
  • Prosopagnosia – damage to facial recognition areas
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10
Q

strokes: resulting from cerebral ischemia (recovery)

A
  • Time-sensitive: treatments that occur in the “sensitive period” quickly post-stroke are more likely to succeed
    • Constraint-induced movement therapy: restraining the “good” arm in order to force you to use the one affected by the stroke -> increases recovery
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11
Q

open-head injuries

A
  • Entry into the brain (ex. By foreign objects like bullets)
  • Ex. Phineas Gage – damage to front of brain damaged pro-social tendencies
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12
Q

2 types of closed-head injuries

A
  • contusion

- concussion

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13
Q

contusions

A
  • Involve damage to the cerebral circulatory system, producing internal hemorrhaging and hematoma
  • Occur when brain slams against skull
  • Contrecoup injuries: the blow causes the brain to strike the inside of the skull on the other side of the head (damage to both sides -> initial is “coup”, second side is “contrecoup”)
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14
Q

concussions

A
  • When there is a blow to the head but no evidence of a contusion or other structural damage
  • Form of Mild Traumatic Brain Injury (MTBI)
  • Cases of chronic traumatic encephalopathy (CTE) suggest that there is long-term damage associated with concussion, even if it is not visible after a single episode
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15
Q

CTE

A
  • Brain damage associated with hitting your head (concussions not necessary to get it -> most are actually sub-concussive)
  • Repeated hits to the head are especially damaging, even if none result in concussions
  • In brains of people with CTE, you’ll find Tau (a protein) and Neurofibrillary Tangles (clumps of tau) -> loss of cell structure -> cell damage/death (unsure if it’s cause of cell death or effect)
  • Symptoms of CTE: paranoia, jealousy, depression, headaches, aggression, mood swings, suicidality, cognitive impairments, motor deficits, etc.
  • Developing techniques to identify CTE while patient is alive (ex. With ligands that bind to tau)
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16
Q

apoptosis

A

programmed cell death; normally a good thing, but too much activity near penumbra causes too much apoptosis (excitotoxicity) which could kill it

17
Q

concussions vs. TBI vs. CTE

A
  • concussions: a syndrome
  • TBI: the event/injury
  • CTE: progressive disease -> will progress whether you have future hits or not
18
Q

distinct profile of cognitive impairments post-stroke

A
  • Studies have previously shown negative impact on attention, memory, language, orientation, visuospatial skills, abstract reasoning, verbal fluency, and executive function, and speed of processing
  • However, more recent studies suggest problems are weighted more toward attention-executive dysfunction rather than memory/language dysfunction
19
Q

types of deficits associated with features of stroke-related damage

A
  • Hemorrhagic stroke, left hemisphere involvement, and recurrence predict subsequent dementia
  • Broca’s aphasia: damage to left posterior, inferior frontal gyrus (limited speech)
  • Wernicke’s aphasia: damage to left posterior, superior temporal gyrus (fluent but meaningless speech)
  • Focal damage leads to selective cognitive impairments
  • Diffuse damage produces more uniform mental slowing and deficits; usually results from an underlying white matter disease (can be seen using DTI)
20
Q

post-stroke interventions

A
  • Compensatory approaches: adapting external environment to altered cognitive abilities
  • Restorative approaches: ex. Repetitive transcranial magnetic stimulation, prism glasses to reduce hemispatial neglect
  • Lowering blood pressure reduces risk of cognitive decline
  • Certain pharmacological agents can benefit cognitive function
  • Increasing physical activity
21
Q

Taupathy

A

neurofibrillary tangles (seen in CTE, Alzheimer’s, and Parkinson’s)

22
Q

TBI

A
  • Likelihood of suffering mild TBIs from collision-heavy sports is high
  • Concussive (symptomatic) or subconcussive (asymptomatic) injuries are both subsets of mild TBI
  • Repetitive mild TBI thought to contribute to development of CTE (correlation exists)
  • The earlier in life you experience TBI, the worse the outcome; TBI is risk factor for dementia
23
Q

Junior Seau

A
  • Experienced multiple concussions; displayed headaches and behavioural changes
  • Post-mortem brain exam showed tau consistent with CTE and scarring from TBI