CVAs motor patterns LMN UMN Exrtrapyramidal cerebellar
localising UMN lesions
Stroke/CVA are very common 4.5 million per annum
1/2 ar ein over 70s and lots of people die soon after
most survivors have disability so stroke is an important cause of diability
stroke
- rapid developing docal neurologica deficit due to a vascualr lesion lasting longer than 24 hours it is important to act, as time is neurons
TIAs
less than 24 hours ( a wee turn) (this is a warning shot) complete recovery - no evidence of infarction ABCDD triage tool for TIA
it is very important
CVA mechanisms
block/ bleed
80% of CVAs are ischaemic look dark on CT
20% are haemorrhage intracerebral or sub arachnoid Look white on CT more global
other causes too but rarer
Ischaemic stroke
thrombisis in 2/3 of cases often in medium sized arteries atherosclosis - plaque rupture
embolism 1/3 of cases
- LA/LV or carotids af risk factor look at chads vasc
In ischaemia neuronal injury from lack of oxygenation and nutritional support leading to damage and death
stop and reverse if we can reperfuse early
decrease damage with neuroprotectant (axtioxidants adn free radical scavengers)
Haemorrhage
- decreased perfusion
- pressure effects
- vasospasm (adjacent ischaemia)
- neuroToxicity from blood and k+ and cellular components
sign symptoms depends of location of lesion weakness is most frequent usualy UMN with localising signs
haemorrage goes beyonf vasculat boundaries
vision can be diabled as well
anterior circualtion vs posterior circulation