Causes of Brain Dysfunction (Part 1) Flashcards
2 types of tumours
- encapsulated
- infiltrating
encapsulated tumours
- Grow between meninges
- “Meningiomas”
- Benign tumours -> can be removed without removing other tissues
infiltrating tumours
- 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
strokes (and tissues affected)
- 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)
2 major types of strokes
- resulting from cerebral hemorrhage
- resulting from cerebral ischemia
strokes: resulting from hemmorhage
- 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)
strokes: resulting from cerebral ischemia (what it is; 3 main causes)
- 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.)
strokes: resulting from cerebral ischemia (3 properties of its brain damage)
- 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
strokes: resulting from cerebral ischemia (types of ischemia-produced damage)
- 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
strokes: resulting from cerebral ischemia (recovery)
- 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
open-head injuries
- Entry into the brain (ex. By foreign objects like bullets)
- Ex. Phineas Gage – damage to front of brain damaged pro-social tendencies
2 types of closed-head injuries
- contusion
- concussion
contusions
- 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”)
concussions
- 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
CTE
- 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)
apoptosis
programmed cell death; normally a good thing, but too much activity near penumbra causes too much apoptosis (excitotoxicity) which could kill it
concussions vs. TBI vs. CTE
- concussions: a syndrome
- TBI: the event/injury
- CTE: progressive disease -> will progress whether you have future hits or not
distinct profile of cognitive impairments post-stroke
- 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
types of deficits associated with features of stroke-related damage
- 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)
post-stroke interventions
- 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
Taupathy
neurofibrillary tangles (seen in CTE, Alzheimer’s, and Parkinson’s)
TBI
- 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
Junior Seau
- Experienced multiple concussions; displayed headaches and behavioural changes
- Post-mortem brain exam showed tau consistent with CTE and scarring from TBI