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Cns Stroke 5th Class.
 

Cns Stroke 5th Class.

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CNS Stroke for 5th year med students.

CNS Stroke for 5th year med students.

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    Cns Stroke 5th Class. Cns Stroke 5th Class. Presentation Transcript

    • CEREBROVASCULAR DISEASE Dr.Mohammad Shaikhani. www.slideshare.net/shaikhani/slideshow
    • Stroke
      • The third most common cause of death in the developed world after cancer &IHD.
      • The most common cause of severe physical disability.
      • The most frequent clinical manifestation of CVD, it may present, particularly in the elderly, as a dementia.
      • ‘ Stroke‘: episodes of focal brain dysfunction due to focal ischaemia or haemorrhage &SAH.
      • Stroke is a common medical emergency with an annual incidence of 180- 300 /100 000.
      • Rises steeply with age the adoption of less healthy lifestyles.
      • 1/5 will die within a month & 1/2 of those who survive will be left with physical disability.
    • ACUTE STROKE
      • 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.
    • Clinical classification of stroke
      • 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.
      • 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.
    • Clinical classification of stroke
      • Several terms used to classify strokes, often based on duration & evolution of symptoms.
      • 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
      • Subdural haematoma
      • Peripheral nerve lesions (vascular or compressive)
      • Cerebral abscess
      • Todd's paresis (after epileptic seizure)
      • Demyelination
      • Hypoglycaemia
      • Encephalitis
      • Conversion disorder
      • Migrainous aura (with or without headache)
      • Focal seizures
    • 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(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 .
    • DIFFERENTIAL DIAGNOSIS OF STROKE& TIA
      • In patients with persisting symptoms , it is necessary to:
      • Confirm the diagnosis.
      • Consider treatments to reverse the underlying pathology.
      • Prevent complications.
      • Alleviate the functional consequences of any persisting neurological impairments .
      • Reduce the risks of further stroke or other vascular events.
    • Classification of Stroke Stroke Primary Hemorrhagic (20% of Strokes) Primary Ischemic (80% of Strokes) Thrombotic 53% Embolic 31% Intracerebral Hemorrhage 10% Subarachnoid Hemorrhage 6%
    • Clinical features
      • 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.
    • Clinical features
      • 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).
    • Clinical features
      • GENERAL EXAMINATION OF STROKE PATIENTS
      • Xanthelasma
      • Rashes (arteritis, splinter haemorrhages, livedo reticularis)
      • Limb ischaemia/deep venous thrombosis
      • Eyes
      • Diabetic changes
      • Retinal emboli
      • Hypertensive changes
      • Arcus senilis
      • Cardiovascular system
      • Blood pressure (hypertension, hypotension)
      • Heart rhythm (atrial fibrillation)
      • Murmurs (sources of embolism)
      • Jugular venous pressure (heart failure, hypovolaemia)
      • Peripheral pulses & bruits (generalised arteriopathy)
    • Clinical features
      • GENERAL EXAMINATION OF STROKE PATIENTS
      • Respiartory system:
      • Pulmonary oedema
      • Respiratory infection
      • Abdomen
      • Urinary retention
      • Locomotor
      • Injuries sustained during collapse with stroke
      • Comorbidities which influence functional abilities
    • Pathology:
      • 85% will have a cerebral infarction due to inadequate blood flow to part of the brain due to atherothrombosis(80% of this 85%), embolism(20% of the 85%) or spasm.
      • The remainder 15% will have had an intracerebral haemorrhage.
      • The combination of severe headache& vomiting at the onset of the focal neurological deficits increases the likelihood of a haemorrhagic stroke.
      • Brain imaging is required to distinguish these pathologies& to guide management.
    • 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 colateral 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.
    • Pathophysiology:
      • 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.
    • Pathophysiology:
      • 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 .
    • Pathophysiology:
      • Higher brain temperature , as might occur in fever&higher blood sugar have 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),
      • Haemorrhagic transformation ccure specially in:
      • Larger infarcts
      • Use of antithrombotic& thrombolytic drugs.
      • Following embolic occlusion when the embolus is lysed by the blood's intrinsic thrombolytic mechanisms.
    • Pathophysiology:
      • 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.
    • ICH:
      • 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
    • INTRACEREBRAL HAEMORRHAGE Pathophysiology:
      • 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
    • INVESTIGATION OF ACUTE STROKE: Aims
      • Confirm the vascular nature of the lesion
      • Distinguish cerebral infarction from haemorrhage.
      • Identify the underlying vascular disease & risk factors.
    • INVESTIGATION OF ACUTE STROKE: Aims
      • Initial investigation of all patients with stroke includes:
      • Simple blood tests to detect common vascular risk factors.
      • An electrocardiogram/Echo.
      • Brain imaging.
      • Markers of rarer causes.
      • Where there is uncertainty about the nature of the stroke, further investigations are usually indicated, especially in younger patients who are less likely to have atherosclerotic disease
    • CAUSES AND INVESTIGATION OF ACUTE STROKE IN YOUNG PATIENTS
    • Cause Investigation Cardiac embolism Echocardiography (including transoesophageal) Premature atherosclerosis Serum lipids Arterial dissection MRI Angiography Thrombophilia Protein C,Protein S,Antithrombin III Homocystinuria) Urinary amino acids,Methionine loading test Antiphospolipid antibody syndrome Anticardiolipin antibodies/lupus anticoagulant Systemic lupus erythematosus Antinuclear antibodies Vasculitis ESR,CRP, (ANCA) CADASIL (Cerebral Autosomal Dominant Ateriopathy with Subcortical Infarcts and Leucoencephalopathy) MRI brain Genetic analysis Skin biopsy Mitochondrial cytopathy Serum lactate Muscle biopsy Neurovascular syphilis Syphilis serology Primary intracerebral haemorrhage Arteriovenous malformation (AVM) Delayed MRI Contrast angiography Drug misuse Drug screen (amphetamine, cocaine) Coagulopathy Prothrombin time (PT) and activated partial thromboplastintime (APTT) Platelet count Subarachnoid haemorrhage Saccular ('berry') aneurysm MRI/angiography AVM MRI/angiography Vertebral dissection MRI/angiography
    • Imaging the brain
      • CT or MRI should be performed in all patients with stroke.
      • Except if the results would not influence management, such as the patient who has a stroke in the latter stages of a terminal illness.
    • Imaging the brain: Brain CT
      • Most practical & widely available.
      • Usually exclude non-stroke lesions, including subdural haematomas & brain tumours.
      • It will demonstrate intracerebral haemorrhage within minutes of stroke onset.
      • 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:CT
      • 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 i.e thrombolytics within 3 hours of symptom onset.
    •  
    • Imaging the brain:MRI
      • 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.
    • 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(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.
    •  
    •  
    • Detecting a cardiac source of embolism
      • 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.
      • Such findings may lead on to specific treatment
    • STROKE IN OLD AGE
      • Incidence: 2/3 of stroke patients are >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 & benefits in those>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: elderly with stroke are more likely to have other pathology such as IHD, HF, COPD, OS, 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& 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
    • MANAGEMENT:SPECIALIST STROKE UNITS
      • Admitting 1000 patients to a stroke unit prevents about 50 patients from being dead or dependent at 6 months
    • GENERAL MANAGEMENT:
      • Management is aimed at:
      • Minimising the volume of brain that is irreversibly damaged, for example thrombolysis by rTPA if presents within the first 3 hours.
      • Preventing complications.
      • Reducing the patient's disability&handicap through rehabilitation.
      • Reducing the risk of recurrent episodes by antiplateletes & statins.
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Airway:
      • Is the patient able to protect his/her airway?
      • Can the patient swallow without evidence of aspiration?
      • Perform a swallow screen & keep patient nil by mouth if swallowing unsafe
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Breathing:
      • Is the patient breathing adequately?
      • Check oxygen saturation & give supplementary oxygen if oxygen saturation < 95%
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Circulation:
      • Are peripheral perfusion, pulse & blood pressure adequate?
      • Treat with fluid replacement, anti-arrhythmics & inotropic drugs as appropriate
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Hydration:
      • Is the patient dehydrated or unable to swallow?
      • Give fluids parenterally or by nasogastric tube if swallow is unsafe
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Nutrition:
      • Assess nutritional status
      • Consider nutritional supplements
      • If dysphagia persists for a day or two, start feeding via a nasogastric tube.
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Medications:
      • If the patient is dysphagic, consider alternative routes for essential medications
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • BP:
      • 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
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Blood glucose:
      • Is the blood glucose ≥11.1 mmol/l (200 mg/dl)?
      • Hyperglycaemia may increase infarct volume, therefore use insulin (via infusion or glucose/potassium/insulin (GKI)) to normalise levels but monitor closely to avoid hypoglycaemia
      • Trials of more rigorous glycaemic control are ongoing
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Tempreture:
      • Is the patient pyrexial?
      • Raised brain temperature may increase infarct volume
      • Investigate & treat any cause but give antipyretics early
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Pressure areas:
      • These should be formally assessed&measures taken to reduce the risk
      • Treat infection, maintain nutrition, provide a pressure-relieving mattress & turn immobile patients regularly
    • GENERAL MANAGEMENT:
      • ACUTE STROKE MANAGEMENT: ADMISSION CHECKLIST
      • Incontinence:
      • Ensure the patient is not constipated or in urinary retention
      • Avoid urinary catheterisation unless the patient is in acute urinary retention or incontinence is threatening pressure areas
    • GENERAL MANAGEMENT:
      • 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 most common with:
      • 1.Lacunar infarction.
      • 2. Enlarging initial lesion, with consequent mass effect, from :
      • A. Expansion of infarction. B. Haemorrhage into an infarction.
      • C. The development of oedema around an infarction.
      • D. Expanding hemorrhage.
      • 3.It is important to distinguish such patients from those who are deteriorating as a result of complications as hypoxia, sepsis, seizures or metabolic abnormalities, more easily reversed.
      • 4. 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:
      • 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
    • Specific medical treatment :
      • 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.
    • Specific medical treatment :
      • 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& has clinically worthwhile effect on long-term outcome; it may be given by rectal suppository or by nasogastric tube in dysphagic patients.
    • Specific medical treatment :
      • Heparin:
      • 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.
    • 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 &other vascular events:
      • The average risk of a further stroke is 5-10% within the first week of a stroke or TIA, 15% in the first year& 5%/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&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 by carotis endartrectomy reduce the overall risk of recurrence, with 5% risk of stroke.
      • Carotid angioplasty& stenting are technically feasible but the long-term effects on the risk of stroke are unclear.
    • Secondary prevention of stroke:
    •