Abrupt loss of function of part of the NS due to a vascular lesion
Brain cells die if deprived of blood supply for four minutes, cerebral necrosis
Brain is 2% of body weight but consumes 20% of absorbed oxygen
Brain has no anaerobic capacity
Anoxia rapidly leads to neuronal necrosis
Focal anoxia / hypoxia leads to CVA or stroke
Global hypoxia / anoxia leads to anoxic encephalopathy
Normal defence mechanisms
Cerebral vasodilation is a response to hypoxia or hypercapnia
Extensive collateral circulation
Cerebral infarct 85%
Intracerebral haemorrhage 7 - 17%
Subarachnoid haemorrhage 5 - 13%
Embolism 3 - 14%
Emboli, detached vegetation from heart valves in sub-acute bacterial endocarditis
May be exacerbated by anaemia
Infarction takes several hours due to compensatory vascular mechanisms.
Oedema around lesions, maximal after about 2 days
Ischaemia may damage vascular endothelium leading to secondary heamorrhage
Necrosed brain tissue undergoes outolysis
Large vessel or lacunar infarcts.
Gender male > female
Race Afro > Asian > White
Previous vascular event
Heart disease, (AF, failure, endocarditis)
Third most common cause of death in the West
1 - 2 per 1000 per year
Incidence increases sharply over the age of 60
Women over 60 years - 17% of deaths
Men over 60 years - 10% of deaths
30 - 40% of patients are alive 3 years after an initial stroke
Transient ischaemic attack (resolves within 24 hours)
Progressive stroke (or stroke in evolution)
Focal deficit of brain function
Headache may precede neurological defect
Onset of stroke is typically over minutes
Effects vary from mild TIAs too coma and complete hemiplegia.
TIAs recover within 24 hours
Loss of consciousness (rare)
Visual field defects
Aphasia or dysphasia may occur if dominant hemisphere is effected. This is usually in the left side of the brain. In right handed people 90% are in the left, in left handed people it is left in approx 60% of individuals.
Other symptoms include epilepsy, receptive dysphasia, giddiness, dysarthria, dysphagia, ataxia and blindness.
Gradual improvement may occur
Clinical history and picture
CT / MRI
Anticoagulation after scanning
Check GCS, care of unconscious patient, check swallowing, aspiration, NBM if swallowing unsafe
Check ventilations, O2 Sats, keep above 95%
Check perfusion of peripheries, are P and BP adequate, possible fluid replacement and correction of heart problems.
Check for dehydration, hydrate using enteral, NG, parenteral
Assess status, give diet, consider supplements, NG feeding for dysphagia
Check swallowing or use other routes
Probably best not to lower BP in first week unless causing specific complications, maintain cerebral perfusion.
Hyperglycaemia may increases infarct volume, give insulin or GKI, watch out for iatrogenic hypoglycaemia
Raised temperature may increase infarct volume, investigate cause of pyrexia, give early antipyuretics
Formally assess risk. Treat infection, give hydration and nutrition.
Position to relieve pressure, prevent disturbance to circulation, support effected limbs, prevent contractures and maintain normal body alignment
Check of constipation and urinary retention. Avoid urinary catheterisation if possible.
Maximise mobility and independence
Aids to communication
Take time to communicate
Prevent complications of immobility
Move patients using proximal holds
Relieve spasticity, prevent contractures, use of walking aids
OT - a range of aids and adaptations
Prevention of arterial disease
Recognise and treat hypertension, diabetes, obesity, hyperlipidaemia
Pharmacology in CVA
Aetiology of thrombosis
Interacting effects of three factors, i.e. Virchow’s Triad.
Disorders of vascular endothelium
Hypertension, atheroma, infection may all lead to endothelial injury.
Blood flow turbulence, underlying collagen will be exposed.
Sluggish or abnormal blood flow
Reduced or turbulent blood flow.
Platelets and other clotting factors have time to accumulate.
Increased blood coagulabilit
Increased proportion of cells to plasma.
Increased red cell count as in hypoxia.
Too many young platelets after haemorrhage.
Low dose aspirin 300mg from day one.
Dipyridamole, alone or with aspirin.
Clopidogrel, reduces primary ischaemic events more than aspirin.
Heparin, side effects outweigh advantages
Thrombolysis in acute presentation, e.g. TPA, alteplase.
Dangerous to give more that 3 hours after onset.
Baclofen acts at spinal level as a GABA derivative to block activation of motor neurones via pre-synaptic receptors.
Correction of haemorrhagic disorders.
Surgery, decompressive crainectomy, carotid endarterectomy
Treat risk factors
ACE inhibitors such as captopril, lisinopril.
Hypoglycaemics, e.g. insulin,
Glibenclamide to stimulate insulin secretion.
Metformin to reduce hepatic gluconeogenesis.
Statins such as simvastatin to lower LDL cholesterol by inhibition of hepatic synthesis.
Omega 3 oils.
Ca++ antagonists such as nifedipine.
Stroke is a clinical term for the acute loss of perfusion to the vascular territories of the brain, leading to ischemia and loss of neurologic function in the affected areas. Resulting from hemorrhagic or ischemic insults, patients present with focal neurologic deficits to hospitals every day. Prompt recognition and treatment are necessary to return blood flow to deprived areas in order to restore neurologic function.
Strokes are grossly divided into ischemic and hemorrhagic types. Ischemic strokes are responsible for roughly 70% of all strokes and occur from thromboembolic occlusion of cerebral arteries. Blood flow occlusion begins an ischemic cascade that, if unchecked, will result in irreversible infarction. Hypoxic-induced cell death causes inflammatory swelling, which may alter the brain architecture, producing a midline shift as shown.
Hemorrhagic strokes are responsible for roughly 30% of all strokes, more commonly from intracerebral rather than subarachnoid etiologies. Patients present similarly to those with ischemic stroke except that they tend to appear more ill with signs of increased intracranial pressure. The most common etiologies are trauma, leakage from small intracerebral arteries secondary to chronic hypertension, aneurysmal rupture, iatrogenic anticoagulation, cocaine abuse, or cerebral amyloidosis.