Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology.
It is further subdivided into ischaemic stroke (caused by vascular occlusion or stenosis) and haemorrhagic stroke (caused by vascular rupture, resulting in intraparenchymal and/or subarachnoid haemorrhage).
Central venous sinus thrombosis is a rare form of stroke that occurs due to thrombosis of the dural venous sinuses.
African-American or Hispanic ancestry
Hx of ischaemic stroke
comorbid cardiac conditions
carotid artery stenosis
sickle cell disease
poor diet and nutrition
illicit drug use
elevated C-reactive protein
aortic arch plaques
Stroke is the third leading cause of death and a major cause of disability in the US  and in England and Wales, and the fourth leading cause of death in Canada. 
In Scotland in 2006 the incident rate for stroke, standardised by age-sex, was 166 per 100,000. 
There are approximately 700,000 new strokes per year. 
Ischaemic stroke accounts for about 85% of cases and haemorrhagic stroke about 15%. 
Ischaemic stroke prevalence can be further sub-divided according to pathophysiological mechanism:
extracranial atherosclerosis (10%)
intracranial atherosclerosis (10%)
lacunar infarction ([small vessel disease] 15%)
indeterminate aetiology ([i.e., cryptogenic] 30%)
other defined causes (10%).
Ischaemic stroke is more common in older people, males, or African-American or Hispanic people. 
The overall incidence of stroke as well as stroke mortality has been decreasing over the last few decades, presumably due to effective primary prevention and management
Ischaemic stroke is a syndrome, not a disease.
It is caused by a transient or permanent critical reduction in cerebral blood flow due to arterial occlusion or stenosis.
Identification of the underlying mechanisms and aetiologies is important so that appropriate therapy can be initiated to decrease the risk of recurrent stroke.
A classification scheme for ischaemic stroke developed for the Trial of Org 10172 in Acute Stroke Treatment (TOAST) provides a framework for determining the stroke mechanism, with implications for identifying the underlying aetiology: 
Large artery atherosclerosis
affects the extracranial carotid or vertebral arteries, or less commonly the major intracranial arteries.
It is a site for thrombus formation that then embolises to distal sites and/or occludes the vessel.
Small vessel (lacunar) stroke
caused by thrombotic occlusion of a small penetrating artery affected by lipohyalinosis (lipid accumulation due to ageing and HTN)
resulting in a <1.5-cm infarct in the perfusion territory of the affected small vessel.
results from thrombus formation in the heart, which then embolises to the intracranial circulation
associated with cardiac disease such as atrial fibrillation.
Accumulating evidence suggests that aortic atherosclerotic plaque is another potential source of thrombus formation with embolism.
Strokes of other determined aetiology
may be caused by various diseases of the intracranial or extracranial vessels (e.g., dissection, vasculitis, venous thrombosis) or haematological system (e.g., sickle cell anaemia, antiphospholipid antibody syndrome, and other hypercoagulable states).
Strokes of indeterminate aetiology
despite complete work-up, are not uncommon.
In the Northern Manhattan Stroke Study, 32% of strokes had no identifiable aetiology. 
vision loss or visual field deficit
sudden onset of symptoms
negative symptoms (i.e., loss of function)
arrhythmias, murmurs, or pulmonary oedema
nausea and/or vomiting
neck or facial pain
miosis, ptosis, and facial anhidrosis (hemilateral)
altered level of consciousness/coma
Regardless of the aetiology, ischaemic stroke occurs when blood supply in a cerebral vascular territory is critically reduced due to occlusion or critical stenosis of a cerebral artery.
A minority of ischaemic strokes are caused by cerebral sinus or cortical vein thrombosis.
These are frequently associated with a prothrombotic (hypercoagulable or hyperaggregable) state, with resulting venous insufficiency and reduced blood flow.
Pathophysiologically, ischaemic stroke can be broadly classified as:
Primary vascular pathologies
(e.g., atherosclerosis, arterial dissection, migraine, or vasculitis)
directly reduce cerebral perfusion and/or result in artery-to-artery embolism
i.e., stenosis or occlusion of a distal artery by an embolus originating in a proximal artery
(e.g., atrial fibrillation, myocardial ischaemia/infarction, patent foramen ovale, aortic arch atherosclerosis)
lead to cerebral arterial occlusion due to embolism
(e.g., prothrombotic hypercoagulable or hyperaggregable states)
directly precipitate cerebrovascular thrombosis (particularly venous), or facilitate systemic venous or intracardiac thrombus formation and cardioembolism.
hypoattenuation (darkness) of the brain parenchyma
loss of grey matter-white matter differentiation, and sulcal effacement; hyperattenuation (brightness) in an artery indicates clot within the vessel lumen
acute ischaemic infarct appears bright on DWI
at later stages, T2 images may also show increased signal in the ischaemic territory
may exclude hypo/hyperglycaemia
may exclude electrolyte disturbance
Serum urea + creatinine
may exclude renal failure
may exclude arrhythmia or ischaemia
may exclude anaemia and thrombocytopenia
may exclude coagulopathy
The goals of treatment of acute ischaemic stroke are to restore blood flow, support energy metabolism in ischaemic tissue, treat complications of stroke-related oedema, and prevent common acute medical complications.
Rapid evaluation and diagnosis is the cornerstone of successful ischaemic stroke therapy.
CT or MRI scan is mandatory to exclude intracerebral haemorrhage and stroke mimics.
The absence of signs on CT does not exclude acute ischaemic stroke.
Following assessment of airway, breathing, and circulation, the next step is to consider whether reperfusion can be achieved.
Following emergency department evaluation and treatment, patients with ischaemic stroke should be transferred to a dedicated stroke unit.
These units have been shown in controlled and non-controlled trials to improve stroke functional outcome and survival.  [B Evidence]
Nutritional support, rehabilitation therapy (physical, occupational and/or speech therapy as indicated), prevention of aspiration (swallowing assessment), and prevention of deep venous thromboembolism (usually with heparin) are all required in the sub-acute phase of hospital care.
Alteplase (tissue plasminogen activator or tPA) promotes thrombolysis and thereby re-canalisation and re-perfusion.[C Evidence]
Based on new clinical trials utilising alteplase for thrombolysis in patients with acute ischaemic stroke and no contraindications, the window of opportunity for treatment of these patients is 4.5 hours after the onset of neurological symptoms.  [A Evidence]
Goal time between emergency department arrival and start of CT scan is 25 minutes, and from emergency department arrival to initiation of intravenous tPA (if indicated) is 60 minutes. 
Decision-makers should be informed of the overall 6% risk of brain haemorrhage, of which approximately half are fatal.
They should also be informed that despite this risk people treated with tPA are more likely to do better.
Overall 1 in 8 people treated with tPA have a complete or near-complete recovery who otherwise would have been disabled; this statistic is the number needed to treat. 
Criteria for treatment:
There is measurable neurological deficit, which does not resolve spontaneously
The symptoms of stroke are not suggestive of subarachnoid haemorrhage
There is no evidence of cerebral venous sinus thrombosis
Onset of symptoms ≤4.5 hours
There is no hx head trauma or prior stroke in the previous 3 months
There is no hx MI in the previous 3 months
There is no hx GI or urinary tract haemorrhage in the previous 21 days
There is no hx major surgery in the previous 14 days
There is no hx arterial puncture at a non-compressible site in the previous 7 days
There is no hx previous intracranial haemorrhage
BP is not elevated at time of infusion (systolic ≤185 mmHg and diastolic ≤110 mmHg);
however, if BP can be pharmacologically lowered and remains stable, then tPA can still be considered if still within the 4.5-hour time window
There is no evidence of active bleeding or acute trauma (fracture) on examination
Not taking an oral anticoagulant or, if anticoagulant being taken, INR ≤1.7
If receiving heparin in previous 48 hours, activated PTT must be in normal range
Platelet count ≥100,000 mm^3
Blood glucose concentration >2.8 mmol/L (>50 mg/dL)
There is no hx seizure with postictal residual neurological impairments
CT does not show a multi-lobar infarction (hypodensity >1/3 volume of cerebral hemisphere)
The patient or family members understand the potential risks and benefits of treatment.
Ischaemic stroke patients should receive aspirin.[B Evidence]
However, if tPA is given, aspirin should not be started for 24 hours, and only then after a head CT shows the absence of intracranial haemorrhage.
Urgent anticoagulation in unselected ischaemic stroke patients, with the goal of improving acute stroke outcomes, is generally not recommended.[B Evidence]
Meta-analyses fail to show reduction in stroke disability in acute ischaemic stroke patients treated with anticoagulants but do show an increase in the risk of haemorrhagic transformation of stroke, particularly in patients with larger stroke volumes. 
Anticoagulation is, however, first-line therapy for cerebral venous sinus thrombosis (as identified on imaging), even in the presence of haemorrhagic transformation of the infarction.
Anticoagulation should be continued for 3 to 6 months.
At the same time as the acute evaluation for reperfusion therapies, steps should be taken to support blood oxygenation,   and systemic BP,  [B Evidence] and to avoid hypo/hyperglycaemia,    and fever.   
These steps, while not shown to be effective by clinical trials, may retard stroke evolution or prevent stroke extension by optimising energy substrate delivery and tissue energy metabolism.
Mortality following ischaemic stroke is 8% to 12%. 
Long-term significant disability, sufficient to impair or prevent return to work, is seen in another 15% to 30%. 
Intravenous thrombolysis and dedicated stroke units are the only interventions shown to improve stroke outcome.
Common medical complications of stroke include aspiration pneumonia, depression, and DVT.
Patients receiving tissue plasminogen activator (tPA)
These patients are more likely to have a better outcome than non-tPA-treated patients, despite the 6% risk of symptomatic intracranial haemorrhage.
The number needed to treat to prevent 1 additional case of stroke-related disability is approximately 8. 
Newer research suggests that the number needed to treat to 'shift' a patient 1 point on the modified Rankin disability scale is even lower:
that is, even in patients without complete or near-complete recovery, tPA probably results in less severe disability.