NEURO Brain Injury Flashcards
(15 cards)
What are congenital brain injuries?
Genetic factors affecting neurodevelopment, pre-natal or birth trauma.
What are traumatic and non- traumatic brain injuries?
->Non- traumatic: long period, e.g. strokes, infections + tumours. Have two main causes.
=Cerebral haemorrhage: blood leaks, get into neuron, toxic to neural tissues. Treatable if aneurism (ruptures to cause issue) spotted early.
=Cerebral Ischaemia: causes lack of oxygen/ glucose, leads to excitotoxicity + neuronal cell death. Blocked blood vessels interrupt blood supply, blocked by plugs (thrombus or embolio) or cardiovascular disease (e.g. atherosclerosis).
-> Traumatic: (intracranial injury), sudden. Specific in focus or widespread. Directly effects tissue or indirectly damaging blood supply system. Closed or open head injuries included.
What are closed and open head injuries?
Closed- no skull penetration . Cerebrospinal fluid cushions the brain, but brain gets moved and bashed into skull, damage can be widespread or diffuse.
-E.g. Dementia Pugillstica (Punch drunk syndrome). Repeated powerful blows, not good for long term brain health. Cumulative structural damage occurs resulting dementia symptoms. Evidence leads to increased likelihood of neurodegenerative disease such as PD + AD.
Open- skull not intact, lead to complications. Object penetrates skull and enters brain. Damage to skull such that bone fragments damage brain tissue. Damage can be localised, risk of other complications (bleeding, infection, swelling) lead to wider damage,
What is a positive and negative of researching damage to circuits?
Can help us understand rest of circuit. But issues with case studies.
Outline Alzheimer’s?
Different to dementia, one of causes of dementia, causes 2/3 dementia. Shrinkage in neurons in brain so enlargement of fluid filled space. 35% of over 85s.
Symptoms= memory loss (selective decline), attention deficits, personality changes.
Intermediate stages: confusion, anxiety, irritability.
Final stages: swallowing and bladder control.
Assessed using MMSE cognitive test.
What is the neuropathological cause of alzheimers?
Shrinkage in brain and accumulation of protein amyloid, compromises the neurons and causes their degeneration.
Plaques in the brain are aggregate lumps of amyloid proteins.
Amyloid precursor proteins (APP) snipped in 2 ways, good and bad. When bad way, causes beta bits to break off + cause build up.
THIS HAPPENS OUTSIDE THE NEURON.
Is there a genetic risk factor?
Yes, appear to have early onset. Versions of apolipropotein E link to Alzheimers. E4 higher likelihood than if you have E2 version, less likely, Links to transport of cholesterol.
How do neurofibrillary tangles effect alzheimers?
Tau.
Neurons contain microtubules in cytoskeleton to keep cell’s shape. Made of Microtubule Associated Proteins (MAP).
Tau gets muddled + tangled.
HAPPENS INSIDE THE NEURON.
Outline Alzheimer’s treatment.
-recent research to get immune system to attack Tau + APP to slow down disease.
-treatments can target additional simultaneous pathological features, loss of neurons that produce/ release neurotransmitter acetylcholine (important for normal cognitive function, e.g. memory).
-> Cholinesterase (AcheE): enzyme breaks down neurotransmitter acetylcholine, stopping it positively effecting neurons. Inhibiting AcheE increase (prolongs) effect of acetylcholine on neuron.
-Blood flow causes tissue environment to worsen causing other areas of Alzheimer’s to also become worse.
What is Parkinson’s Disease?
Involuntary tremulous motion, lessened muscular power, stooped posture. Affect 0.5% population (1-2% OAP) 2.5x more common in men.
-idiopathic disease: which means as far as we know each case has its own origin (no single cause).
-intensely studied, no cure but one of the most understood brain disease.
What are Parkinson’s symptoms?
Spontaneous movement, insufficient movement, bradykinesia- slow movements, increased muscle tone- rigidity, resting tremor- looks like pill rolling, shuffle gait + flexed posture, impaired balance, mask like expression. Issues with initiation and selection of movement not movement itself.
How does the basal ganglia link to parkinsons?
Lack of dopamine in nigrostriatal dopamine pathway, found in basal ganglia is linked to Parkinson’s.
Especially key as 80% brain dopamine is in basal ganglia.
Caused by dopamine producing cells dying off.
Basal ganglia key in selecting motor skills so not trying to do 50 things at once. In Parkinson’s inhibition fails to be turned off. Normally burst of dopamine stops inhibition, so motor system keeps going.
What are some ways we can prevent the basal ganglia from being stuck ‘on’?
-lesions in globus pallidus in basal ganglia- only possible in very severe cases.
-prescribe levo dopa, can’t just give dopamine cause doesn’t cross blood brain barrier.
-apomorphine + cannabis (dopamine agonist)
-deprenyl (monoamine agonist).
-electrical stimulation of basal ganglia (deep brain stimulation)
How does deep brain stimulation work as treatment for Parkinson’s?
Targets same site as lesion with electrical current tuned to shut them down (inhibit output), reversible, controllable/ adjustable. Rapidly becoming more effective.
