Stroke and sub-arachnoid haemorrhage

Stroke

WHO definition- neurologicla deficit of sudden onset, w/ focal rather than global dysfunction, in which symptoms presumed to be of no-traumatic vascular origin and last for >24hrs
110,000 people have first stroke each year w/ 7% per aunnum risk of further stroke
- 10,000 people <55yrs, 1000<30yrs
3rd leading cause of death (67,000/year)
pathological classification:
- cerebral infarct - 81%
- primary intracerebral haemorrhage - 10%
- SAH - 5%
- other - 5%

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mean CBF 50ml/100g/min
- 10-20ml/100g: electrical failure, penumbra part of injury (ischaemic but still functional)
- <10ml/100g: metabolic failure, core part of injury
- penumbra is progressively recruited to core- 1.9million neurones lost/min
mechanisms of infarct:
- large artery atherothrombosis
  - cholesterol plaque rupture (acute clot superimposed on chr. stenosis)
- cardioembolic stroke- e.g. from AF
- lacunar strokes
  - occlusion of small, perferator arteries; involves deep white matter and brainstem
  - RFs: HTN, DM, hyperlipidaemia
- cryptogenic strokes
- other: carotid dissection, vasculitis, endocarditis
CT- infarcts are dark (low attenuation), difficult to see initially (loss of grey/white matter differentiation, sulcal effacement), develops over period of days, eventually well demarcated and dark- same as ICH strokes

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mechanisms
- primary (80%)
  - chronic HTN, amyloid angiopathy (+amyloid deposits in vessels)
- secondary
  - vascular abnormalities (AVM, aneurism, cavernoma "berry appearance", venous angioma)
  - tumour
  - impaired coagulation (e.g. warfarin Rx)
  - vasculitis
  - drug induced
CT
- bright 'high attenuation' due to Hb content
- immediate appearance but becomes isodense after a few days
- oft surrounded by low attenuation area of oedema and necrosis
- mass effect is common (midline shift etc)

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infarc of small penetrating art in pons and basal ganglia or deep (subortical) haemorrhage
- contralat hemiplegia
- contralat hemisensory loss
- contralat upgoing plantar
- NO cortical signs (hemianopia, dysphasia, apraxia, neglect)
assoc w/ chronic HTN

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Posterior cerebral artery infarct or occipital haemorrhage
- often unnoticed by pt
- contralat homonymous visual field defect (b/c CNII lesion before chiasm)
cerebellar infarction/haemorrhage
- nausea, vomiting, loss of balance, vertigo, headache
- DANISH- Dysdiadochokinesis & Dysmetria (past-pointing), ipsilat Ataxia, Nystagmus, Interntion tremor, Scanning dysarthria, Heel-shin incoordination
- risk of obstructive hydrocephalus and coma
basilar artery occlusion
- bi/unilat CN palsies
- severe quadriplegia
- bilat upgoing plantars
- coma, resp arrest
- locked in syndrome: complete m. paralysis except upward gaze

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stroke syndrome resolves <24hrs
- mean carotid territory TIA - 14mins
- mean vertebral artery TIA - 8mins
10% will have stroke in next 90 days (5% in next 2 days)
sudden onset of focal signs
- motor, expressive dysphasia, amaurosis fugax
  - amaurosis fugax: retinal art occlusion, transient monocular blindness 1-5mins, moves peripheral to centre, painless (headache-migraine or temporal arteritis)
- hemianopias, hemisensory symtpoms
- diplopia, vomiting, vertigo, dysarthria, dysphagia, ataxia
almost never cause:
- global symptoms (e.g. syncope, dizzines)
- migrainous symtpoms (headache, visual disturbances)
- buring or pain in limbs
- recurrent falls
- seizure-like symptoms

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causes:
- ruptured aneurysm (85%)
- perimesencephalic (10%)
- rare causes (5%)
  - Wegner's, dissection, AVM, cavernoma, sickle cell disease, coagulopathies, tumours, cocaine, warfarin
thunderclap headache (85-100%)
- any location, onset to peak w/in 5 min
- DDx- meningitis, venous thrombosis, ischaemic stroke, acute HTN crisis
assoc features
- vomiting (75%)
- depressed consciuosness (67%)
- precipitating factor (20%)- sex, exercise
- subhyaloid haemorrhage (14%)
- neck stiffness
- preceeding headache

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