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Acute stroke is characterised by the rapid appearance (usually over minutes) of a focal deficit of brain function, most commonly a hemiplegia with or without signs of focal higher cerebral dysfunction (such as aphasia), hemisensory loss, visual field defect or brain-stem deficit.
Provided that there is a clear history of a rapid-onset focal deficit, the chance of the brain lesion being anything other than vascular is 5% or less
Care needs to be taken to exclude other differential diagnoses if the symptoms progress over hours or days&could be explained by causes other than focal cerebral dysfunction.
Confusion, memory or balance disturbance may reflect focal deficits but are more often due to other causes.
Several terms used to classify strokes, often based on duration & evolution of symptoms.
Transient ischaemic attack (TIA): strokes in which symptoms resolve within 24 hours, indicating that underlying cerebral haemorrhage or extensive cerebral infarction is extremely unlikely. The term TIA traditionally also includes patients with transient monocular blindness ( amaurosis fugax), usually due to a vascular occlusion in the retina.
Transient symptoms, such as syncope, amnesia, confusion& dizziness, which do not reflect focal cerebral dysfunction, are often mistakenly attributed to TIA.
Stroke: those events in which symptoms last more than 24 hours. The differential diagnosis of both TIA/stroke is similar.
Clinical classification of stroke
Progressing stroke (or stroke in evolution). a stroke in which the focal neurological deficit worsens after the patient first presents. Such worsening may be due to increasing volume of infarction, haemorrhage or related oedema.
Completed stroke. This describes a stroke in which the focal deficit persists& is not progressing.
DIFFERENTIAL DIAGNOSIS OF STROKE& TIA
Primary cerebral tumours
Metastatic cerebral tumours
Peripheral nerve lesions (vascular or compressive)
Todd's paresis (after epileptic seizure)
Migrainous aura (with or without headache)
DIFFERENTIAL DIAGNOSIS OF STROKE& TIA
In clinical practice, it is probably most important to distinguish those patients with strokes who, when seen, have persisting focal neurological symptoms, from those whose symptoms have resolved.
When assessing a patient within hours of symptom onset, it is not possible to distinguish stroke from TIA unless the symptoms have already resolved.
In those without persisting symptoms, the emphasis should be on confirming the diagnosis&preventing further vascular events .
DIFFERENTIAL DIAGNOSIS OF STROKE& TIA
In patients with persisting symptoms, it is necessary to:
Confirm the diagnosis.
Consider treatments to reverse the underlying pathology.
Alleviate the functional consequences of any persisting neurological impairments .
Reduce the risks of further stroke or other vascular events.
The clinical assessment provides an estimate of the site of the lesion (i.e. which arterial territory is involved)& its size, both of which will have a bearing on management, such as suitability for carotid endarterectomy.
The neurological deficits can be identified from the patient's history &if these are persistent, from the neurological examination.
The presence of a unilateral motor deficit, higher cerebral function deficit (e.g. aphasia or neglect) or a visual field defect usually places the lesion in the cerebral hemisphere.
Ataxia, diplopia, vertigo and/or bilateral weakness usually indicate a lesion in the brain stem or cerebellum.
Different combinations of these deficits can define several stroke syndromes which reflect the site & size of the lesion& may provide clues to underlying pathology.
and complications of the stroke
Reduced conscious level usually indicates a large-volume lesion in the cerebral hemisphere but may result from a lesion in the brain stem or complications such as obstructive hydrocephalus, hypoxia or severe systemic infection.
Clinical assessment of the patient with a stroke should also include a general examination, since this may provide clues to the cause of the stroke& identify important comorbidities.
Peripheral pulses and bruits (generalised arteriopathy)
GENERAL EXAMINATION OF STROKE PATIENTS
Injuries sustained during collapse with stroke
Comorbidities which influence functional abilities
Of patients presenting with a stroke, 85% will have sustained a cerebral infarction due to inadequate blood flow to part of the brain atherothrombosis, embolism or spasm.
The remainder 15% will have had an intracerebral haemorrhage.
Brain imaging is required to distinguish these pathologies and to guide management.
The combination of severe headache and vomiting at the onset of the focal neurological deficits increases the likelihood of a haemorrhagic stroke.
Pathophysiology Cerebral infarction is a process which takes some hours to complete, even though the patient's deficit may be maximal close to the onset of the causative vascular occlusion.
After the occlusion of a cerebral artery, the opening of anastomotic channels from other arterial territories may restore perfusion to its territory.
Similarly, a reduction in perfusion pressure leads to compensatory homeostatic changes to maintain oxygenation.
These changes can sometimes prevent even occlusion of a carotid artery from having any clinically apparent effect.
If & when these homeostatic mechanisms fail, the process of ischaemia starts and ultimately leads to infarction.
As the cerebral blood flow declines, different neuronal functions fail at various thresholds.
Once blood flow falls below the threshold for the maintenance of electrical activity, neurological deficit appears.
At this level of blood flow, the neurons are still viable; if the blood flow increases again, function returns and the patient will have had a transient ischaemic attack,but if the blood flow falls further, a level is reached at which the process of cell death starts.
Hypoxia leads to an inadequate supply of adenosine triphosphate (ATP), which in turn leads to failure of membrane pumps, thereby allowing influx of sodium and water into the cell (cytotoxic oedema)& the release of the excitatory neurotransmitter glutamate into the extracellular fluid.
Glutamate opens membrane channels, allowing the influx of calcium and more sodium into the neurons.
Calcium entering the neurons activates intracellular enzymes that complete the destructive process.
The release of inflammatory mediators by microglia and astrocytes produces death of all cell types in the area of maximum ischaemia.
The infarction process is worsened by the anaerobic production of lactic acid& consequent fall in tissue pH.
Attempts to produce 'neuroprotective drugs' to slow down the processes leading to irreversible cell death have so far been largely disappointing .
The final result of the occlusion of a cerebral blood vessel therefore depends upon the competence of the circulatory homeostatic mechanisms, and the severity and duration of the reduction in blood flow.
Higher brain temperature, as might occur in fever, and higher blood sugar have both been associated with a greater volume of infarction for a given reduction in cerebral blood flow.
If ischaemic damage has occurred to the vascular endothelium, subsequent restoration of blood flow may cause haemorrhage into the infarcted area (so-called haemorrhagic transformation).
This is particularly likely to occur in larger infarcts, in patients given antithrombotic and thrombolytic drugs, and possibly following embolic occlusion when the embolus is lysed by the blood's intrinsic thrombolytic mechanisms
Radiologically, a cerebral infarct can be seen as a lesion which comprises brain tissue that is ischaemic and swollen but recoverable (the ischaemic penumbra), as well as dead brain tissue that is already undergoing autolysis.
The infarct swells with time and is at its maximal size a couple of days after the stroke onset.
At this stage it may be big enough to exert some mass effect both clinically and radiologically.
As the weeks go by, the oedema subsides and the infarcted area is replaced by a sharply defined fluid-filled cavity.
This usually results from rupture of a blood vessel within the brain parenchyma: a primary intracerebral haemorrhage.
It may also occur in a patient with a subarachnoid haemorrhage if the artery ruptures into the brain substance as well as into the subarachnoid space or vice versa.
Haemorrhage frequently occurs into an area of brain infarction; if the volume of haemorrhage is large, this may be difficult to distinguish from primary intracerebral haemorrhage both clinically and radiologically.
INTRACEREBRAL HAEMORRHAGE CAUSES &ASSOCIATED RISK FACTORS Disease Risk factors Complex small vessel disease with disruption of vessel wall Age Hypertension Amyloid angiopathy Familial (rare) Age Impaired blood clotting Anticoagulant therapy Blood dyscrasia Thrombolytic therapy Vascular anomaly Arteriovenous malformation Cavernous haemangioma Substance misuse Alcohol Amphetamines Cocaine
The explosive entry of blood into the brain parenchyma causes immediate cessation of function in that area as neurons are structurally disrupted and white matter fibre tracts are split apart.
The haemorrhage itself may expand over the first minutes or hours or it may be associated with a rim of cerebral oedema, which, along with the haematoma, acts like a mass lesion to cause progression of the neurological deficits.
If big enough, this can cause shift of the intracranial contents, producing transtentorial coning and sometimes rapid.
If the patient survives, the haematoma is gradually absorbed, leaving a haemosiderin-lined slit in the brain parenchyma
Investigations in acute stroke: Diagnostic question Investigation Is it a vascular lesion? CT/MRI Is it ischaemic or haemorrhagic? CT/MRI Is it a subarachnoid haemorrhage? CT Lumbar puncture Is there any cardiac source of embolism? Electrocardiogram (ECG) Echocardiogram What is the underlying vascular disease? Duplex ultrasound of carotids Magnetic resonance angiography (MRA) CT angiography (CTA) Contrast angiography What are the risk factors? Full blood count Cholesterol Blood glucose Is there an unusual cause? ESR Clotting/thrombophilia screen
INVESTIGATION OF ACUTE STROKE
Aims to confirm the vascular nature of the lesion, distinguish cerebral infarction from haemorrhage and identify the underlying vascular disease and risk factors.
Initial investigation of all patients with stroke includes a range of simple blood tests to detect common vascular risk factors and markers of rarer causes, an electrocardiogram and brain imaging.
Where there is uncertainty about the nature of the stroke, further investigations are usually indicated.
This especially applies to younger patients who are less likely to have atherosclerotic disease
CAUSES AND INVESTIGATION OF ACUTE STROKE IN YOUNG PATIENTS
Brain imaging with either CT or MRI should be performed in all patients with stroke.
Exceptions to this include patients in whom the brain scan results would not influence management, such as the patient who has a stroke in the latter stages of a terminal illness.
CT is the most practical and widely available method of imaging the brain.
It will usually exclude non-stroke lesions, including subdural haematomas and brain tumours.
It will demonstrate intracerebral haemorrhage within minutes of stroke onset. However, especially within the first few hours after symptom onset, CT changes in cerebral infarction may be completely absent or very subtle, though changes usually evolve over time.
Imaging the brain
For most purposes, a CT scan performed within the first day or so is adequate for clinical care but there are certain circumstances in which an immediate CT scan is essential.
Even in the absence of changes suggesting infarction, abnormal perfusion of brain tissue can be imaged with CT after injection of contrast media (i.e. perfusion scanning).
This can be useful in guiding hyper-acute treatment of ischemic stroke.
Imaging the brain
MRI is not as widely available as CT, scanning times are longer and it cannot be used in some individuals with contraindications
MRI diffusion weighted imaging (DWI) can detect ischaemia earlier than CT, and other MRI sequences can also be used to demonstrate abnormal perfusion.
MRI is more sensitive than CT in detecting strokes affecting the brain stem and cerebellum, and unlike CT, can reliably distinguish haemorrhagic from ischaemic stroke even several weeks after the onset.
CT and MRI may reveal clues as to the nature of the arterial lesion. For example, there may be a small, deep lacunar infarct indicating small vessel disease, or a more peripheral infarct suggesting an extracranial source of embolism.
In a haemorrhagic lesion, the location might indicate the presence of an underlying vascular malformation, saccular aneurysm or amyloid angiopathy.
Imaging the brain
INDICATIONS FOR AN IMMEDIATE CT/MRI IN ACUTE STROKE
Patient on anticoagulants or with abnormal coagulation
Plan to give thrombolysis or immediate anticoagulants
Deteriorating conscious level or rapidly progressing deficits
Suspected cerebellar haematoma, to exclude hydrocephalus
Imaging blood vessels:
Many ischaemic strokes are caused by atherosclerotic thromboembolic disease of the major extracranial vessels.
Detection of extracranial vascular disease can help establish why the patient has had an ischaemic stroke and may, in highly selected patients, lead on to specific treatments including carotid endarterectomy to reduce the risk of further stroke.
The presence or absence of a carotid bruit is not a reliable indicator of the degree of carotid stenosis.
Extracranial arterial disease can be non-invasively identified with duplex ultrasound, MR angiography (MRA) or CT angiography .
Because of the significant risk of complications, intra-arterial contrast angiography is reserved for patients in whom non-invasive methods have provided contradictory or incomplete information, or in whom it is necessary to image the intracranial circulation in detail: for example, to delineate a saccular aneurysm, an arteriovenous malformation or vasculitis.
Detecting a cardiac source of embolism
Approximately 20% of ischaemic strokes are thought to be due to embolism from the heart.
The most common causes of cardiac embolism are atrial fibrillation, prosthetic heart valves, other valvular abnormalities & recent MI.
These can often be identified by clinical examination and ECG.
Cardiac sources of embolism can exist without obvious clinical or ECG signs.
A transthoracic or transoesophageal echocardiogram can be useful, either to confirm the presence of a clinically apparent cardiac source or to identify an unsuspected source such as endocarditis, atrial myxoma, intracardiac thrombus or patent foramen ovale.
Such findings may lead on to specific treatment
STROKE IN OLD AGE
Incidence: two-thirds of stroke patients are aged over 60 years.
Diagnosis: a clear history is as important in older people as in younger patients, but will be more difficult to obtain if there is pre-existing cognitive impairment or communication difficulties.
Thrombolysis: very few data are available concerning the risk and benefits in patients over 80 years.
Carotid endarterectomy: the benefits accrue quickly after transient stroke; therefore, when it is indicated, advanced age alone is not a contraindication to surgery.
Comorbidities: older patients with stroke are more likely to have other pathology such as ischaemic heart disease, cardiac failure, chronic obstructive pulmonary disease (COPD), osteoarthritis and visual impairments. All will have to be addressed as part of overall management.
STROKE IN OLD AGE
Cognitive impairment: adversely affects outcome, as much of rehabilitation involves the learning and retention of new skills.
Over-diagnosis of recurrent stroke: the reappearance of neurological signs from a previous stroke in a patient who has other acute systemic illness or is hypotensive may be incorrectly attributed to a new event.
Diffuse small-vessel cerebrovascular disease: very common, and may present insidiously with gait abnormalities and/or significant memory impairment. It also predisposes to confusional states when intercurrent infection or metabolic disturbance supervenes.
Anticoagulation for secondary prevention after stroke: may be indicated in certain circumstances, but must be used with caution because the associated risks in frail older patients are higher due to comorbidity, falls, cognitive impairment and interaction with other medication.
STROKE complications: Complication Prevention Treatment Chest infection Nurse semi-erect Antibiotics Avoid aspiration Physiotherapy Epileptic seizures Maintain cerebral oxygenation Anticonvulsants Avoid metabolic disturbance Deep venous thrombosis/pulmonary embolism Maintain hydration Early mobilisation Anti-embolism stockings Heparin (for high-risk patients only) Anticoagulation (exclude haemorrhagic stroke first) Painful shoulder Avoid traction injury Physiotherapy Shoulder/arm supports Local corticosteroid injections Physiotherapy Pressure sores Frequent turning Nursing care Monitor pressure areas Pressure-relieving mattress Avoid urinary damage to skin Urinary infection Avoid catheterisation if possible Antibiotics Use penile sheath Constipation Appropriate aperients and diet Appropriate aperients Depression and anxiety Maintain positive attitude and provide information Antidepressants
SPECIALIST STROKE UNITS
Admitting 1000 patients to a stroke unit prevents about 50 patients from being dead or dependent at 6 months
Management is aimed at:
Minimising the volume of brain that is irreversibly damaged,
Reducing the patient's disability&handicap through rehabilitation.
Reducing the risk of recurrent episodes.
Early admission to a specialised stroke unit facilitates coordinated care from a specialised multidisciplinary team&has shown to reduce both mortality& residual disability amongst survivors.
Consideration of a patient's rehabilitation needs should commence at the same time as acute medical management.
Dysphagia is common after stroke&can be detected by an early bedside test of swallowing, which allows hydration, feeding & medication to be given safely, if necessary by nasogastric tube or IV.
In the acute phase it may be useful to refer to a checklist to ensure that all the factors which might influence the patient's outcome have been addressed.
The deteriorating stroke patient:
The patient's neurological deficits may worsen during the hours or days after their onset.
This is probably most common amongst those with lacunar infarction but may occur in other patients, due to extension of the area of infarction, haemorrhage into it or the development of oedema with consequent mass effect.
It is important to distinguish such patients from those who are deteriorating as a result of complications such as hypoxia, sepsis, epileptic seizures or metabolic abnormalities which may be more easily reversed.
Patients with cerebellar haematomas or infarcts with mass effect may develop obstructive hydrocephalus& some will benefit from insertion of a ventricular drain &/or decompressive surgery.
The deteriorating stroke patient:
Some patients with large haematomas or infarction with massive oedema in the cerebral hemispheres may benefit from anti-oedema agents, such as mannitol, artificial ventilation and/or surgical decompression to reduce intracranial pressure, although evidence for the effectiveness of these interventions is still incomplete
Specific medical treatment :
Thrombolysis & other revascularisation treatments:
Intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) increases the risk of haemorrhagic transformation of the cerebral infarct with potentially fatal results.
However, if given within 3 hours of symptom onset to highly selected patients, the haemorrhagic risk may be offset by an improvement in overall outcome.
Alternative methods of revascularisation, including intra-arterial thrombolysis, mechanical dissolution or removal of the thrombus, are used but little evidence is available concerning the balance of risks / benefits.
Specific medical treatment :
Aspirin Aspirin (300 mg daily) should be started immediately after an ischaemic stroke unless rt-PA has been given, in which case it should be withheld for at least 24 hours.
Aspirin reduces the risk of early recurrence and has a small but clinically worthwhile effect on long-term outcome; it may be given by rectal suppository or by nasogastric tube in dysphagic patients.
Specific medical treatment :
Formal anticoagulation with heparin has been widely used in treating acute ischaemic stroke in the past.
Whilst this does reduce the risk of early ischaemic recurrence and venous thromboembolism, these benefits are offset by a definite increase in the risk of both intracranial and extracranial haemorrhage&routine use of heparin does not result in better long-term outcomes, and therefore it should not be used in the routine management of acute stroke.
It is unclear whether anticoagulation with heparin might provide benefit in selected patients, such as those with recent myocardial infarction, arterial dissection or progressing strokes.
Intracranial haemorrhage must be excluded on brain imaging before considering anticoagulation.
Specific treatment for haemorrhagic stroke :
Coagulation abnormalities, most commonly due to oral anticoagulants, should be reversed as quickly as possible to reduce the likelihood of the haematoma enlarging.
Promising research suggests that, in highly selected patients, haematoma enlargement may be reduced by the early administration of recombinant factor VII even in patients without a clotting problem.
Reducing the risk of further strokes :
Reducing the risk of further strokes and other vascular
The average risk of a further stroke is 5-10% within the first week of a stroke or TIA, perhaps 15% in the first year and 5% per year thereafter.
The risks are not clearly different for intracerebral haemorrhage.
Patients with ischaemic events should be put on long-term antiplatelet drugs &statins to lower cholesterol.
For patients in atrial fibrillation the risk can be reduced by about 60% by oral anticoagulation to achieve an INR of 2-3.
The risk of recurrence after both ischaemic and haemorrhagic strokes can be reduced by blood pressure reduction, even for those with blood pressures in the normal range.
Carotid endarterectomy & angioplasty :
A small proportion of patients with a carotid territory ischaemic stroke or TIA will have a greater than 70% stenosis of the carotid artery on the side of the brain lesion.
Such patients have a greater than average risk of stroke recurrence.
For those without major residual disability, removal of the stenosis has been shown to reduce the overall risk of recurrence, although the operation itself carries a 5% risk of.
Carotid angioplasty and stenting are technically feasible but the long-term effects on the risk of stroke are unclear.