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.
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.
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.
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.
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
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.
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.
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.
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.
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.
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
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.
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
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.
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.