Stroke is an acute neurological deficit caused by cerebrovascular aetiology lasting >24 hours.
It is further subdivided into ischaemic stroke and haemorrhagic stroke.
Ischaemic stroke is due to occlusion or critical stenosis of a cerebrospinal artery
Haemorrhagic stroke is due to rupture of a cerebrospinal artery, resulting in intraparenchymal and/or subarachnoid haemorrhage.
Intracerebral haemorrhage is further subdivided into primary and secondary aetiology.
Primary or spontaneous intracerebral haemorrhage is defined as haemorrhage in the absence of vascular malformations or associated diseases.
Secondary intracerebral haemorrhage is from an identifiable vascular malformation or as a complication of other medical or neurological diseases that either impair coagulation or promote vascular rupture.
black and/or Hispanic
FHx of haemorrhagic stroke
cerebral amyloid angiopathy
autosomal dominant mutations in the COL4A1 gene
hereditary haemorrhagic telangiectasia
autosomal dominant mutations in the KRIT1 gene
autosomal dominant mutations in the CCM2 gene
autosomal dominant mutations in the PDCD10 gene
illicit sympathomimetic drugs
heavy alcohol abuse
Stroke is the third most common cause of death in most resource-rich countries and is a major cause of disability.
Worldwide, around 4.5 million people die each year from stroke. 
In the US, there are approximately 700,000 new strokes per year. 
Ischaemic stroke accounts for about 85% of cases and haemorrhagic stroke for about 15%.
Three quarters of haemorrhagic strokes are intracerebral haemorrhage, with the rest being subarachnoid haemorrhage.
The incidence of intracerebral haemorrhage rises with age and is increased in certain groups, including men, black people, and people of Hispanic ethnicity
Cerebral small vessel disease, caused by chronic HTN or cerebral amyloid angiopathy, accounts for the large majority of primary intracerebral haemorrhage.
Cerebral amyloid angiopathy is caused by beta-amyloid deposition in the walls of medium-sized and small arteries restricted to the brain. 
Rare hereditary cases may be due to genetic mutations in cystatin-C, amyloid precursor protein, or transthyretin. 
Cerebral amyloid angiopathy is a major cause of lobar haemorrhage but is not a cause of haemorrhage in other intracranial locations.
HTN and vascular malformations can cause haemorrhage in any intracranial location.
Secondary intracerebral haemorrhage arises from an identifiable vascular malformation or as a complication of other medical or neurological diseases that either impair coagulation or promote vascular rupture.
Aetiologies include cerebral infarction or cerebral tumour with haemorrhage into the diseased tissue, sympathomimetic drugs of abuse such as cocaine, and diseases causing impaired coagulation such as haematological malignancies or liver disease.
An exception is that most experts consider anticoagulation-associated haemorrhage to be a form of primary intracerebral haemorrhage.
FHx of haemorrhagic stroke
hx of vascular malformations
hx of chronic HTN
cerebral amyloid angiopathy
hx of atrial fibrillation
hx of liver disease
autosomal dominant mutations in the COL4A1, KRIT1, CCM2, or PDCD10 genes
hx of haematological disorder
altered level of consciousness/coma
Intracerebral haemorrhage is caused by vascular rupture with bleeding into the brain parenchyma.
The expanding haematoma may shear additional neighboring arteries, resulting in further bleeding and haematoma expansion. 
Eventually haematoma growth is halted by a combination of haemostasis and increased pressure.
Significant haematoma growth (30% to 40% increase) over several hours following presentation is common in those who present within 3 to 4 hours of the onset of symptoms. 
The period of bleeding may be extended even longer in anticoagulated patients.
Arresting haematoma growth is therefore a key objective for medical or surgical therapies.
As a consequence of haematoma growth, the haemorrhage may rupture into the subarachnoid space or the intraventricular space.
Mortality is increased when intraventricular haemorrhage is present, in part due to the associated increased risk of communicating or non-communicating hydrocephalus. 
Mortality from intracerebral haemorrhage is high and may result from direct destruction of critical brain areas, compression of critical brain areas by adjacent haematoma, or cerebral circulatory arrest caused by globally increased intracranial pressure
signs of myocardial ischaemia, cerebral T waves
Controlled clinical trials have shown that admission to a dedicated stroke unit, in comparison with admission to a general medical or surgical service, is associated with improved survival and less disability at 1 year.  [A Evidence]
Stroke units have multidisciplinary teams including physicians, nursing staff, and rehabilitation consultants.
Improved supportive care, avoidance of complications such as infection, and earlier initiation of rehabilitation therapy are among the mechanisms stroke units have that are hypothesised to produce better outcomes.
Studies of stroke units have predominantly included ischaemic stroke patients, but it is reasonable to infer that haemorrhagic stroke patients also receive benefit.
Blood glucose control
DVT prophylaxis as long as no evidence of continued bleeding
Anti-pyrexia if necessary
Facilities are to have 24-hour availability of emergency neurosurgical consultation due to the potential need for surgical intervention.
Most patients are often admitted to an ICU due to the frequent need for tracheal intubation or invasive monitoring of BP or intracranial pressure.
Consensus opinion is that surgical resection of cerebellar haemorrhage is life-saving and is recommended if the patient is drowsy or clinically unstable, or if the haemorrhage is large (>3 cm).
For supratentorial haemorrhage (i.e., haemorrhages arising in the cerebrum, excluding the cerebellum and brainstem), a large randomised controlled trial (RCT) failed to determine a benefit of surgery. 
Surgery for cerebellar haemorrhage has never been studied in an RCT, however.
Caution is exercised in patients with prolonged severely depressed level of consciousness, who tend to have poor outcomes with or without surgery.
However, with clinical decompensation, patients may be considered for surgical evacuation.
Early resection within 12 hours may help prevent neurological damage but may also be associated with recurrent bleeding.
Mortality is significantly higher than for ischaemic stroke, in the range of 35% to 40%. 
Only 20% to 30% of all patients are well enough to live independently by 3 to 6 months.
Haemorrhage volume is the strongest predictor of outcome.
Advanced age, impaired consciousness at presentation, and rupture of the haematoma into the ventricular system are also associated with worse outcomes. 
A similar score (the FUNC score) can be used to predict 3-month functional outcomes. 
While unproven, guidelines recommend maintenance of normal tissue oxygenation, avoidance of hypotension, maintenance of normal body temperature, and control of hyperglycaemia to prevent secondary injury to vulnerable tissue. 
In many cases, life-sustaining measures (e.g., mechanical ventilatory support) are stopped because of perceived futility of continued care.