View stunning SlideShares in full-screen with the new iOS app!Introducing SlideShare for AndroidExplore all your favorite topics in the SlideShare appGet the SlideShare app to Save for Later — even offline
View stunning SlideShares in full-screen with the new Android app!View stunning SlideShares in full-screen with the new iOS app!
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 ( as aphasia), hemisensory loss, visual field defect or brain-stem deficit.
A clear history of a rapid-onset focal neurological deficit, makes the chance of a 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.
Confusion, memory or balance disturbance may reflect focal deficits but are more often due to other causes.
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.
In clinical practice, it is probably most important to distinguish those patients with strokes who, when seen, have persisting focal neurological symptoms(Stroke), from those whose symptoms have resolved(TIA).
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 or TIA, the emphasis should be on confirming the diagnosis&preventing further 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 &/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 co morbidities& complications of the stroke.
Syndromes of acute stroke. Total anterior circulation syndrome-TACS (A). Partial anterior circulation syndromes-PACS (B, C, D and E). Pure motor stroke-lacunar syndrome (F). Posterior circulation syndromes-POCS (G, H, I, J and K).
If & when these homeostatic mechanisms fail, the process of ischaemia starts& 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& the patient will have had a TIA, but if the blood flow falls further, a level is reached at which the process of cell death & stroke starts.
Hypoxia leads to an inadequate supply of (ATP), leading to failure of membrane pumps, allowing influx of sodium & 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 & more sodium into the neurons.
Calcium entering the neurons activates intracellular enzymes that complete the destructive process.
The release of inflammatory mediators by microglia &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.
‘ Neuroprotective drugs' to slow down these processes have been disappointing .
Radiologically, a cerebral infarct is seen as a lesion which comprises brain tissue that is ischaemic& swollen but recoverable (the ischaemic penumbra), as well as dead brain tissue that is already undergoing autolysis.
The infarct swells with time& is at its maximal size a couple of days after the stroke onset, may be big enough to exert some mass effect both clinically & radiologically.
As the weeks go by, the oedema subsides& 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.
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& 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& 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& sometimes rapid death.
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
Not widely available , scanning times are longer &cannot be used in some individuals with contraindications.
MRI diffusion weighted imaging (DWI) can detect ischaemia earlier than CT & other MRI sequences can also be used to demonstrate abnormal perfusion.
It is more sensitive than CT in detecting strokes of brain stem/ cerebellum& unlike CT, can reliably distinguish haemorrhagic from ischaemic stroke even several weeks after the onset.
CT/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.
Haemorrhage location might indicate the presence of an underlying vascular malformation, saccular aneurysm or amyloid angiopathy.
Many ischaemic strokes are caused by atherosclerotic thromboembolic disease(A-A) of the major extracranial vessels.
Detection of extracranial vascular disease can help establish why the patient has had an ischaemic stroke & 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.
20% of ischaemic strokes are thought to be due to embolism from the heart.
The most common causes of cardiac embolism are AF, prosthetic heart valves, other valvular abnormalities & recent MI.
These can often be identified by clinical examination &ECG, but 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.
Cognitive impairment: adversely affects outcome, as much of rehabilitation involves the learning& 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&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 & 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
Unless there is HF or renal failure, evidence of hypertensive encephalopathy or aortic dissection, do not lower the blood pressure in the first week since it will often return towards the patient's normal level within the first few days
Early blood pressure reduction may decrease cerebral perfusion & increase infarction to offset potential benefits.
Trials of early blood pressure lowering are ongoing
5.Some patients with large cerebral hemispheres haematomas or infarction may benefit from anti-oedema agents;mannitol, artificial ventilation&/or surgical decompression to reduce intracranial pressure, although evidence for the effectiveness of these interventions is still incomplete
Thrombolysis & other revascularisation treatments:
IV thrombolysis (rt-PA) increases the risk of haemorrhagic transformation of the cerebral infarct with potentially fatal results,but 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.
Reduce the risk of early ischaemic recurrence & venous thromboembolism, but there is definite increase in the risk of both intracranial & extracranial haemorrhage&routine use does not result in better long-term outcomes, so 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.