Stroke and transient ischaemia attack (TIA) are both cerebrovascular events that are commonly encountered in clinical practice due to abnormal perfusion of cerebral tissue.
A stroke can be broadly defined as:
“A clinical syndrome characterised by sudden onset of rapidly developing focal or global neurological disturbance, which lasts more than 24 hours or leads to death”
A TIA can be broadly defined as:
“Transient ( < 24 hrs) neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without evidence of acute infarction”
Traditionally, symptom resolution within 24 hours was diagnostic of TIA. However, a significant proportion (1/3rd) of patients whose symptoms resolve in 24 hours have evidence of infraction (i.e. a stroke) on imaging. Consequently, the definition now incorporates the phrase ‘without evidence of acute infarction’.
Strokes are extremely common within the UK with the total number of strokes each year estimated to affect 110,000 people.
Approximately 230 per 100,000 people will develop a first-ever stroke each year and 50 per 100,000 will have a first-ever TIA. In England and Wales up to 80,000 people are admitted with an acute stroke each year and the collective mortality from a first-ever stroke is 11%.
Strokes can be classified into two major types: Haemorrhagic or Ischaemic.
Haemorrhagic strokes are the result of bleeding within the brain parenchyma, ventricular system or subarachnoid space. Haemorrhagic strokes account for approximately 15% of all strokes. They are further divided into an intracerebral haemorrhage (ICH) or subarachnoid haemorrhage (SAH).
Due to the different presentation and management pathway, a SAH is usually discussed separately and will not be discussed further here.
Ischaemic strokes are the result of occlusion to blood vessels that supply the brain parenchyma leading to infarction (tissue necrosis secondary to ischaemia). Ischaemic strokes are common accounting for 85% of all strokes.
Ischaemic strokes may be further sub-classified according to the Bamford/Oxford classification (Discussed further below).
Haemorrhagic strokes are the result of bleeding into the brain parenchyma whereas ischaemic strokes are the result of occlusion to cerebral vessels.
Occlusion to cerebral vessels in ischaemic strokes is the result of thrombus (atheromatous plaque) within a vessel or an embolus (blood clot) arising from a distant site. Both bleeding or occlusion represent a final common pathway that leads to the development of a stroke. There are severel precipitants for the development of bleeding or occlusion.
The most common cause of a haemorrhagic stroke is hypertension. Other causes include arteriovenous malformations (AVM) and trauma.
Ischaemic strokes are caused by conditions that precipitate atherosclerosis development (thrombosis) or result in emboli.
In TIA, there is usually a brief reduction in blood flow related to ischaemia to an area of cerebral tissue that causes neurological symptoms.
TIA's are most commonly due to conditions that cause emboli formation (i.e atrial fibrillation, carotid artery disease).
Stroke risk factors generally share similarities with cardiovascular risk factors. They relate to conditions that affect the integrity of blood vessels.
Stroke and TIA present with sudden neurological deficit. The clinical features correlate with the territory that has been affected.
The clinical features of a haemorrhagic stroke are largely dependent on the area of the brain that is involved. Furthermore, they are more likely to present with global features such as headache and altered mental status.
The clinical features of an ischaemic stroke are broadly based on location (anterior cerebral circulation versus posterior cerebral circulation).
Anterior ischaemic strokes lead to a constellation of features dependent on the extent and location of the stroke. These include weakness/sensory loss, visual changes and higher cerebral dysfunction.
Posterior ischaemic strokes are more likely to involve balance issues, visual problems, and have cranial nerve involvement. This is because the posterior circulation comes from the vertebra-basilar arterial distribution and supplies the brainstem, cerebellum and occipital cortex. They account for 20-25% of ischaemic strokes.
*ipsilateral cranial nerve lesions with contralateral sensory & motor limb deficits
A TIA is suggestive by sudden neurological deficit that have resolved within 24 hours. The typical clinical features suggestive of a TIA include:
The Bamford/Oxford system sub-classifies ischaemic strokes by the presenting clinical features, which correlates with the cerebral territory that has become infarcted.
These refer to a collection of syndromes with characteristic clinical features also known as ‘brainstem syndromes’.
One commonly discussed posterior stroke syndrome is lateral medullary syndrome or ‘Wallenberg’ syndrome. This is the result of occlusion to the posterior inferior cerebellar artery (PICA), which affects the lateral aspect of the medulla oblongata. It causes a classical constellation of clinical features including nystagmus, vertigo, ipsilateral Horner’s syndrome, ipsilateral facial sensory loss, dysarthria and dysphagia in association with contralateral loss of pain and temperature.
The diagnosis of stroke and TIA should be suspected clinically based on history and examination.
Patients suspected of having a stroke based on clinical features should be referred urgently to a specialist stroke centre (i.e. HASU; hyperacute stroke unit). Here, patients can have urgent cross-sectional imaging (i.e. CT head).
Patients suspected of having a TIA will have a normal examination as the neurological features will have resolved. Therefore, the history is essential in the diagnosis. Patients with suspects TIA will be further investigated according to the local TIA pathway (discussed further below).
The Face Arm Speech (FAST) test is often used as a rapid diagnostic assessment in the community. The presence of one or more of new facial weakness, arm weakness or speech difficulty is considered a positive test.
There are a number of conditions, which may mimic the features of a stroke.
Common culprits include migraines, hypoglycaemia, peripheral vestibular diseases, seizures, Todd’s paresis (focal weakness following a seizure), acute confusion or peripheral neuropathies (i.e Bell’s palsy).
The key investigation for suspected stroke is a CT head, which should be undertaken as soon as possible in all patients.
The indications for urgent CT head (within an hour) in patients with a suspected acute stroke include:
A CT head is very sensitive for detecting cerebral haemorrhage. In an ischaemic stroke, CT imaging is usually normal in the first few hours, and a normal CT head in the presence of neurological symptoms is presumed secondary to ischaemia.
These additional investigations are important in the work up of patients presenting with a stroke or TIA
The NIH Stroke Scale is scoring system out of 42, which has been designed as a predictive score of clinical outcomes. A patient with a score of <4 is likely to have a good clinical outcome.
This scoring system can be completed on initial assessment as part of the work-up for suspected acute stroke. A NIHSS score is important in the consideration of thrombolysis. A high score (> 22) indicates a significant proportion of the brain is affected by ischaemia, and as such, there is higher risk of cerebral haemorrhage following treatment. A score > 26 is often considered a contraindication to thrombolysis.
Any patient suspected of having an acute stroke should be referred urgently to a hospital with specialist stroke service that can facilitate stroke thrombolysis if required.
The key to management is first to determine whether the stroke is haemorrhagic or ischaemic on the initial CT.
The management of an acute intracerebral bleed depends on the extent of the bleed and the clinical state of the patient including co-morbidities and suitability for neurosurgical intervention if required.
With most small bleeds, there is no requirement for neurosurgical intervention. This usually includes small deep haemorrhages, haemorrhage without hydrocephalus or rapid neurological deterioration, a low GCS (< 8) not secondary to haemorrhage, posterior fossa haemorrhage or significant comorbidities prior to stroke.
In all patients, coagulation defects should be reversed using vitamin K or prothrombin complex concentrates. If the risk of thrombosis is excessively high then consideration of an IVC filter should be addressed.
If the CT head does not reveal any signs of intracerebral bleeding then the patient is managed as an ischaemic stroke.
An initial decision should be made about whether the patient would be suitable for thrombolysis. Thrombolysis is the intravenous administration of synthetic tissue plasminogen activator (i.e. Alteplase), which is a powerful thrombolytic (clot-busting) drug. There are a number of contraindications to thrombolysis would should be assessed and the timeframe in which it should be administered for maximum benefit is 4.5 hours. This is known as the ‘thrombolysis window’.
If Thrombolysis is not appropriate, patients should be started immediately on 300 mg of aspirin for two weeks after an intracerebral haemorrhage has been excluded. After the two week period, patients can be converted to secondary prophylaxis with 75 mg clopidogrel unless anti-coagulation (i.e. warfarin, apixban) would be more appropriate because of the aetiology (e.g. AF). If thrombolysis was given, aspirin is usually started 24-48 hours following treatment.
The management of TIA is based on the ABCD2 scoring system. This is a prognostic score to identify people at high risk of stroke after TIA.
Patients with a suspected TIA should be started on 300 mg of aspirin and referred to a TIA clinic is based on severity. If the ABCD2 score is ≥ 4 they should be assessed within 24 hours. If the score is < 4 they should be assessed within 7 days. If patients present more than 7 days following the episode they should be assessed within 7 days. Any patient presenting with crescendo TIA (2+ in a week) should be considered for urgent inpatient assessment.
Following initial treatment of acute stroke, management consists of ongoing monitoring, secondary prevention (i.e. blood pressure control, blood glucose control) and rehabilitation.
Treatment with anti-hypertensive medications is only recommended if there is a hypertensive emergency with subsequent complication.
Maintain a blood glucose concentration between 4-11 mmol/litre.
Patients should be commenced on a statin 48 hours after the initiation of a stroke unless already established on one in which case it can be continued.
Following 2 weeks of aspirin therapy, patients should be considered for definitive secondary prevention anti-platelet or anti-coagulation therapy depending on the aetiology of the stroke.
Strokes secondary to suspected carotid artery disease (i.e. anterior circulation strokes) require carotid artery imaging and consideration of carotid endarterectomy. Typically, surgery is considered when there is carotid stenosis of 50-99% or 70-99% with stable neurological symptoms.
All patients should have an initial swallowing and nutritional assessment on admission. If unsafe, patients should be made nil by mouth. Where appropriate, patients may require nutritional support in the form of supplements, specialist dietary advice and/or tube feeding.
Patients require early mobilisation and specialist input from occupational and physical therapists.
Complications of stroke can be broadly divided into early complications and late complications.
Term used to describe rapid neurological deterioration due to the effects of space occupying cerebral oedema following middle cerebral artery (MCA) territory stroke.
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