- Mechanisms of Stroke
- Cerebral infarct
- Brainstem Infarct
- Lacunar Infarct
- Hypertensive Encephelopathy
- Multi-infarct dementia
- Weber’s Syndrome
- Cerebral Haemorrhage
- Stroke Rehabilitation
- Related Articles
Stroke is a sudden onset of brain dysfunction, caused by an alteration in cerebrovascular blood supply. It is characterised by:
- Rapid, acute onset – within a few minutes
- Focal neurological defect – almost always some sort of hemiplegia, with/without other focal neurological signs
- If these two instances are true, then there is a 95% chance there is a vascular cause. Be wary if the symptoms get worse over hours/days, as this points to another cause.
Stroke is often a clinical diagnosis – confirmed with imaging
- Haemorrhage – 10-20%
- Brain Ischaemia (Infarct) – 80-90%
- Other type of embolism
- Systemic hypoperfusion
- TIA – Transient Ischaemic Attack
- This is essentially a ‘minor’ stroke. It may present with stroke like symptoms (limb weakness, dysphagia, visual defects), but the clinical effects will completely resolve within 24 hours. They are usually the result of micro emboli, (80%)but not always. Sometimes a mass lesion may mimic a TIA, and other times, they are the result of a temporary reduced blood flow – e.g. with massive postural hypotension, or decreased blood flow through a stenosed artery – which is later compensated for by autoregulation mechanisms.
- Completed Stroke
- The clinical effects have reached their maximum – usually within 6 hours of the onset.
- Stroke in evolution
- Describes the progress of a stroke in the first 24 hours
- Mortality – 20% in first 2 months, then roughly 10%/year
- <40% of stroke (not TIA) patients make a full recovery
- Drowsyness at presentation has a poor prognosis
Mechanisms of Stroke
- Arterial embolism – from a distant site; e.g. carotids, vertebral or basilar arteries. The embolus will occlude an artery of the brain resulting in infarction. May also come from heart valves in endocarditis.
- Haemorrhage – can be in the cerebrum itself, or also a subarachnoid haemorrhage may cause a similar effect
- Venous infarct
- Carotid/vertebral dissection
- Fat / air embolism – e.g. in divers
- MS – a demyelinating plaque may act as an embolus
- Mass lesions (e.g. tumour)
- Thrombocythaemia and thrombophilia
- Drugs – particularly cocaine and OTC cold remedies that contain vasoconstrictors.
Damage will occur when the blood flow to brain tissue drops below 50% of the normal value. Remember in some (probably elderly patients) there will already be reduced blood flow, e.g. to due stenosis/atherosclerosis, so this is not ‘50% of the patients normal bloodflow’, but 50% of the normal value.
- 10/1000 per year(!) at age 75
- The 3rd most common cause of death in the developed world – accounts for 12% of all deaths.
- More common in black Africans than in Caucasians.
- More common in men
- Uncommon before the age of 40
- 25% of stroke patients will die of the condition
- Most strokes occur in the morning – the blood pressure is lowered during the night whilst asleep, but on waking, the BP rises, and is now more likely to dislodge any embolism.
These are very similar the same as those for cardiovascular disease:
|Hypertension||Damages arterial walls, and thus leads to increased risk of thrombus formation, and haemorrhage.||Treat with drugs / lifestyle||↑↑||↑↑||↑|
||Increases BP, as well as direct effects on arterial walls. Stopping reduces risk by 50% in the first year, and is indistinguishable from non-smoker after 5 years.||Stop||↑↑||↑||↑|
|Exercise and Diet||Recommended 30-60 mins exercise 4-6x per week||Increase activity, reduce fat intake||↑||↔||↔|
|Atrial Fibrillation||Increases the chances of thrombus formation in the heart||Anticoagulate||↑||↔/↑||↔|
|Diabetes||Increases risk of high BP and atherosclerosis||Treat / Control||↑||↔||↔|
|↑Cholesterol||Increases risk of atherosclerosis. Treatment will recue risk by 1/3, even in those with normal cholesterol levels!||Statins||↑||↔||↔|
|Carotid artery Stenosis||Usually seen on angiogram of head/neck||Surgery (stenting)||↑↑||↔||↔|
|Ethnicity||Black Africans, and Asians at higher risk – probably due to increased risk of diabetes in these population||–||↑||↔||↔|
|Age||>65. The biggest risk factor for stroke||–||↑↑||↑||↑|
|Valvular heart disease|
|Sex (Male)||Men are more likely to have strokes, and when they do, they are more likely to cause damage|
|Cerebral aneurysm||Rupture of this can cause haemorrhage||↔||↑↑||↔|
- Cerebral infarct
- Cerebral Haemorrhage
- Subarachnoid haemorrhage
Note that low dose aspirin has no proven beneficial effect, and in fact, high usage of cox-II inhibitors increases the risk.It is also now thought that low dose oestrogen (e.g. in the contraceptive pill), does not significantly increase the risk in otherwise healthy women.
CADASIL – a rare, inherited cause of stroke and vascular dementia. Caused by a defective NOTCH3 gene. There are multiple small infarcts in the brain. Often presents as migraine and depression in teenagers, and by the 20’s and 30’s there are often TIA’s and strokes. Dementia may follow after age 40-50.
- Symptoms completely resolve within 24 hours
- 80% due to thromboembolus
- Site of damage can be roughly located from clinical signs:
Likely thrombus from carotid system
Most likely affecting cerebral function
Likely thrombus from vertebrobasilar system
Most likely affecting Cerebellar/Brainstem Function
|Aphasia/dysphasia||Diplopia, vertigo, vomiting|
|Hemiparesis||Swallowing difficulties / dysarthria|
|Amaurosis fugax*||Hemianopic visual loss|
|Sensory loss (hemi)||Sensory loss (hemi)|
|Hemianopic visual loss||Transient global amnesia**|
* Amaurosis fugax – this is a sudden loss of vision in one eye, caused by an infarct in the retinal artery(ies). You can sometimes see the obstruction on ophthalmoscopy, which is useful clinically, as the same symptoms is seen in migraine – where the arteries will always appear normal. Thus if a defect is visible, it is highly likely to be the result of a TIA
**Transient global amnesia – this involves an episode of amneia, that usually occursin those over 65, and completely resolves within 24 hours. Unlikely to happen more than once in the same patient.
Diagnosis of TIA
Usually clinical, few investigations required
Check the following:
- Carotid bruit
- ECG – check for underlying arrhythmia, particularly AF
- Valvulalr heart disease – echo not necessary unless history suggestive
- Recent MI
- Check radial/radial delay, and difference in brachial pressures between right and left.
- A difference of more than 20mmHg between arms suggests subclavian artery stenosis.
Check for underlying conditions / RF’s:
- Postural hypotension
- Lowcardiac output / bradycardia / AF / arrhythmia
- Antiphospholipid syndrome
Differentials for TIA
- Mass lesions – very difficult to differentiate clinically
- Epilepsy – often had limb jerking, and symptoms will have onset over a few mins, as opposed to the instant effect in TIA.
- Migraine – may cuase similar symptoms, in which case confusion, and characteristic visual disturbance (e.g. zig-zag pattern) are usually present. TIA is unlikely to cause headache, or comparable visual defects.
Prognosis for TIA
5 years after TIA:
- 30% of patients have a stroke (of these, 30% occur within the first year)
- 15% have MI
TIA in the anterior circulation is more serious than TIA in the posterior circulation.
Investigations and management
Usually symptoms resolve in 24 hours. If not, or if you suspect something more serious, then follow the same protocol as for stroke; detailed below.
Otherwise, patients are often admitted to hospital on the basis of their ABCD2 score. This score predicts the likelihood of a further CVA event. A patient with a score of ≥4 should be admitted to hospital for investigation within 24 hours. A patient with a score of ≤3 can be investigated as an outpatient – but should still have investigations within 1 week.
Follow-up investigations typically include:
- Carotid doppler scan – to check the level of carotid artery stenosis. A level of >60% usually required a carotid endarterectomy to reduce future stroke risk
- ECG – if not already done
- Bloods – if not already done – including FBC, U+Es, cholesterol
- Consider echocardiogram – to check for a cardiac source of emboli if any suggestive history (not always indicated)
- Consider brain imaging – if not already done or if concerns about symptoms (not always indicated)
- If requesting these investigations as an outpatient (e.g. by GP or by Emergency Doctor before discharge) then patient should be referred to a neurologist / TIA clinic for follow up
- High dose aspirin (300mg) should be given once diagnosis is confirmed – usually after CT has confirmed there is no haemorrhage stroke (if symptoms have resolved then almost certainly has been ischaemic rather than haemorrhagic)
- Continue 100mg daily aspirin thereafter
The clinical impact is very varied, and depends on both the size of the infarct, and the location. They can vary from infarcts that result in death, to ones that are completely clinically silent. TIA is somewhere in the middle.
- Estimating the effected region via clinical signs alone is inaccurate.
- 60% – Atherosclerosis of the carotid arteries and aortic arch
- 20% – valvular heart disease
- 20% – disease of the vessels in the brain itself
The most common stroke presentation is in a branch of the middle cerebral artery – affecting the internal capsule. A similar set of signs will be caused by internal carotid occlusion. In these cases there is:
- Limbs usually floppy, and reflexes reduced/absent
- Facial weakness (not always)
- Hemianopia – visual field defect in which vision is lost in half of the visual field in one/both eyes.
- Aphasia – when the dominant hemisphere is affected
- Important to ask about left and right handedness!
- These symptoms usually develop rapidly, over a period of minutes, or less commonly they can develop over a few hours.
Not usually any headache – there are no pain receptors within the brain itself
Not usually any LOC
VERY RARE – epileptic seizure at the time of onset.
- The symptoms are usually maximal just after the time of onset. Recovery will occur gradually over days, weeks and even months. The longer has passed since the stroke, the less chance of recovery.
- Reflex will return early on, but often become exaggerated, with an extensor plantar response.
If there is headache and/or impaired consciousness then the cause is likely to involve some sort of swelling, and thus if the onset is acute, it is likely to be haemorrhagic.
When examining a patient for stroke, you should perform a ‘general examination’ to check for clues as to the origin of the lesion:
- Diabetic changes
- Retinal emboli
- Hypertensive changes
- Arcus senilis (corneal arcus)
- BP – checking for both hypo/hypertension
- Murmurs – valvular disease can throw off emboli
- JVP – heart failure
- Peripheral bruses and bruits – shows general arteriopathy
- Pulmonary oedema
Abdomen – feel bladder for urinary retention
Sudden cessation of blood supply to neurons, lead quickly to hypoxic cells. This causes:
- The Na+/K+ pump to fail, and Na+ begins to accumulate in the cell
- This excess Na+ changes the osmotic balance, and more liquid enters the cell, causing oedema.
- The oedema is highly significant. In the direct area around the infarct, the cells will die very quickly, as they swell and burst. Burst But in an area around this, there are cells that have odema, but that can be saved. The whole basis of treatment is to save these oedema cells. This area is known as the penumbra.
- As many of the cell swell and burst, there is an increase in intracranial pressure which can further affect the blood supply to the area, resulting in a vicious circle.
- Another factor in the accumulation of Na+ within a cell is the continued depolarisation of neurons in the affected area. This is because the reuptake process for glutamate is dependent on ATP, and without O2 there is no ATP, so glutamate remains present in the synaptic regions, and cells remain depolarised.
- This mechanisms of cell damage, as a result of prolonged depolarisation of the cell, is known as EXCITOTOXICITY.
- Excitotoxicity also results in the failure of AMPA and NMDA receptors, which allows excessive levels of calcium into the cell. This allows:
- the release of free radicals – which also lead to necrosis in the area.
- the production f cytokines, which causes inflammation – adding to the oedema and general tissue swelling in the region.
- Ca2+ can also directly lead to apoptosis in the penumbra.
Anterior Cerebral artery
Weak leg (± shoulder), on the contralateral side
Middle Cerebral Artery
Posterior Cerebral Artery
Carotid and Vertebral Artery Dissection
Accounts for just under 20% of strokes in those under 40, and is often the result of trauma. There may be symptoms resembling stroke, TIA, or migraine, with pain at the site of the dissection.
These can result in wide varying, and complex symptoms, depending on which nuclei are involved, and if the involvement is bi or unilateral.
Examples of clinical features:
|Sensory Loss||Medical lemniscus / spinothalamic tract|
|Facial Numbness||5th nerve nuclei|
|Facial weakness||7th Nerve nucleus|
|Nystagmus and vertigo||Vestibular connections|
|Dysphagia / dysarthria||9th/10th nuclei|
|Horner’s syndrome||Sympathetic fibres|
|Altered consciousness||Reticular formation|
There are several particular recognised patterns of brainstem stroke:
Wallenberg’s syndrome / lateral medullary syndrome / posterior inferior cerebellar artery thrombosis (PICA) – all mean the same thing. Presents with acute vertigo and other cerebellar signs. Due to the nature of the cerebellar pathways, there are the following signs:
- Spinothalamic sensory loss
- Hemiparesis (usually mild, quite rare)
- Facial numbness (V)
- Diplopia (VI)
- Horner’s syndrome
- 9th and 10th nerve lesions
Coma – from a stroke affecting the reticular activating system
The locked-in syndrome – the patient is aware and awake, but virtually all motor neurons are paralysed, and thus the patient cannot move. Usually the eyes are the only structures not affected. Caused by an upper brainstem infarct.
Pseudo bulbar palsy – the result of a lower brainstem infarct. Results in bilateral impairment of the 9-12th cranial nerves. There is dysarthria and dysphagia.
Infarcts in the deep arteries of the brain, may account for up to 25% of ischaemic strokes. They can be seen on MRI, and are commonly noted at autopsy.
Often it is symptomless
it may present with very localised symptoms – as the infarct affects a very localised part of the brain, such as purely sensory symptoms, or purely motor symptoms.
- Hemisensory loss
- Unilateral ataxia
Encephelopathy literally means ‘damage to the brain’, in this case, as the result of malignant hypertension. This hypertension can result in TIA’s, stroke, and more rarely, subarachnoid haemorrhage. There is commonly papilloedema, which can be due to either of the main causes:
- direct infarct affecting the optic nerve
- infarct in other part of the brain, resulting in odema, which then puts pressure on the optic disc.
- Usually the brain swelling in this instance is the result of many small infarcts, which have caused the brain to enlarge.
Anton’s Syndrome – Infarct affecting on the visual cortex
May present with hemianopic visual loss, and no other features. Can be distinguished from pathology of the optic nerve due to the fact that the visual field is affected.
The result of an infarct on one side of the midbrain, it presents with:
- Ipsilateral III nerve paralysis
- Contralateral hemiplegia
CT and MRI
Infarctions will always show up as a wedge shape on both CT and MRI.
Haemorrhage – blood appears bright white (dense) on CT – but the longer it has been present, the darker it becomes. After 1-2 weeks it may be indistinguishable from brain tissue.
- It is possible to roughly estimate the length of time the haemorrhage has been present by the density of the blood on a scan.
- Depending on the site of the bleed, it will have a different shape on the scan
The damage is easier to see the longer it has been present
- For example, a ‘new’ stroke (e.g. <2 hours old) may not show up at all, but after 6-12 hours will be clearly visible. This has clinical consequences – because the sooner you can see the stroke, the sooner you can treat it.
Diffusion MRI scans – these detect abnormalities much earlier than on normal MRI and CT – especially in the case of infarction. Thus they are useful to confirm the diagnosis earlier than can be achieved with other methods.
- This type of MRI exploits the fact that damaged cells fill with water – and thus contain more water than normal cells in the early stages of damage.
Looks at the blood vessels in the head and neck. To distinguish the blood vessels when looking at one of these scans:
- Vertebral artery is often the smallest of the main 3
- The internal carotid has no branches
- The external carotid has branches
This test can show areas of stenosis and thrombus formations. It is also useful for looking for aneurysms.
If carotid stenosis is present, then 80% of these patients will benefit from surgery, if they are fit enough to undergo it.
You may want to perform a carotid Doppler as a cheaper and easier alternative to look for carotid stenosis.
Hypertension – this is common in early stroke, and generally untreated. If other signs point towards malignant/underlying hypertension (e.g. large heart on CXR, retinopathy), then consider management.
ECG – checking for AF as a source of emboli. If present, treat accordingly
CXR – checking the size of the heart (hypertension) and particularly the size of the left ventricle (AF). If you are particularly concerned, you may also want to do an echocardiogram.
Bloods –basically to rule out other differentials:
- ↑ESR – with episodes of headache, and tender scalp (can be anywhere on the scalp) – points towards giant cell arteritis.
- FBC/platelets/clotting – looks for the presence of bleeding disorders
- Glucose – low glucose could have caused feelings of faintness, and LOC, also diabetes is a RF
- Cholesterol/Lipids – RF for stroke
Pretty much indistinguishable clinically from infarct, although:
- More likely to lose consciousness
- More likely to have headache (usually sudden onset)
- Neurological defects are usually sudden (like embolic stroke) but are more likely to be progressive.
Haemorrhages are nearly always the result of uncontrolled chronic hypertension.
- Use of cocaine can cause cerebral haemorrhage acutely
- Aneurysm (often congenital), AV malformation, clotting disorders and tumours are also worth bearing in mind.
The blood will collect around the brain tissue and compress local areas, resulting in neurological dysfunction. Large bleeds can increase intracranial pressure enough to cause herniation of the brainstem, and/or further infarcts in the midbrain and pons. It is this mechanism that is likely to cause loss of consciousness. Blood can also leak into the ventricular system, causing acute hydrocephalus.
CT and MRI
- Acute blood – will show up as bright white – because it is more dense than the surrounding tissue. The longer the blood has been present, the darker its colour will become, until eventually you may not be able to distinguish it very easily from the surrounding brain tissue.
- This occurs because the longer the blood is present, the more of its products are broken down and removed, and thus its density is reduced. Macrophages in particularly will break down blood products.
- Note that any dense abnormality in the brain is blood until proven otherwise.
General Emergency Measures
- Maintain airway
- Prevent hypoxia
Treat fever / source of fever
Treat hypo / hyperglycaemia – this can help to limit the extent of damage
Ensure good nursing care to prevent bed sores
As soon as you are confident of the diagnosis of ischaemic stroke or TIA, and the patient has no contra-indications, you should initiate treatment. Thrombolysis is under-used in the UK – probably due to doctors fears that there may be haemorrhage present.
Contra-indications for thrombolysis
In reality, many patients will have contra-indications for thrombolysis, and thus is cannot be used. Instead, they should be offered:
Aspirin – 300mg/day for 2 weeks, then 75mg day
- Be wary asthma and GI bleeds
- If aspirin hypersensitive, give clopidogrel
Dipyridamole – should also be given if ischaemia confirmed by CT / MRI.
The use of warfarin should be considered once the cause is known (i.e. if AF, or if definite thrombosis). Treatment range s usually an INR of 2-3.
Carotid endartectomy – is also considered in many patients. Those with carotid obstruction of >60% are generally considered.
Treatment is essentially supportive. If anticoagulants and antiplatlets have been given, then the effect can be reversed with vitamin K, fresh frozen plasma (FFP) and platelet transfusions.
- Hypertension should only be treated if systolic is >185 mm Hg
If the haemorrhage causes a mass of >3cm diameter, then surgery can be lifesaving.
Determine the objectives
- What was the previous level of function?
- E.g if they couldn’t walk before the stroke, then they are not going to be able to walk after it!
Physiotherapy – helps to prevent spasticity and contractures. Also teaches patients how to cope with their current level of function
- Looks at levels of function, and teaches patient how to cope. Also arranges home alterations (stair lifts, hand rails etc) to help the patient stay living at home.
Preventing strokes in those who have never had one before
- Control Risk factors (hypertension, obesity, lipids, cholesterol, diabetes smoking)
- Anticoagulation – lifelong therapy for those with rheumatic heart disease or prosthetic valves, or AF
Preventing another stroke in previous sufferers.
- Control risk factors – controlling BP and cholesterol greatly reduces the risk, even if they aren’t particularly raised to begin with!
- Anticoagulation – if embolic stroke, then aspirin or warfarin. Combining aspirin with clopidogrel or another antiplatelet agent reduces risk further.