Cerebral amyloid angiopathy (CAA) is characterised by the deposition of Aß proteins in the media and adventitia of small and mid-sized cortical and leptomeningeal arteries (and, less frequently, veins). It is a component of any disorder in which amyloid is deposited in the brain, and it is not associated with systemic amyloidosis. The prevalence of CAA increases with advancing age. Some autopsy series have found CAA in 5% of individuals in the seventh decade but in 50% of those older than 90 years. While often asymptomatic, CAA is being increasingly recognised as an important cause of ICH in the elderly, accounting for up to one-fifth of all spontaneous ICH in this group. We present an 82 year-old gentleman who was diagnosed with cSAH and fulfilled the criteria for probable CAA

Most patients with suspected stroke should be transported without delay to a hospital, which has access to the required diagnostic tests and appropriate hyperacute treatments 24 h/day and 7 days/week. Once admitted, patients should be managed in a stroke unit rather than a general medical ward. There appears to be no systematic increase in length of hospital stay associated with organized (stroke unit) care. The recent development of hyperacute stroke units is not based on evaluation within RCTs but appears to improve processes of care in the acute phase. Processes of care on a stroke unit should mirror those found to be effective in RCTs. Stroke care should be specialized, organized, and multidisciplinary (i.e. provided by medical, nursing, physiotherapy, occupational therapy, speech therapy, and social work staff who are interested and trained in stroke care). The other beneficial components of organized stroke care are likely to be many, but it remains uncertain which are the most effective. Early discharge from the stroke unit with support from a domiciliary rehabilitation team (coordinated by the stroke unit) promises to reduce hospital length of stay and improve rehabilitation in the home and patient outcome.

Aneurysmal SAH is a severe disease, and the post-haemorrhage period fraught with potential complications that must be recognized and treated early for favourable outcome. While diagnosis of SAH is often straightforward from clinical history and initial CT, some patients will require cerebrospinal fluid evaluation. The aneurysm must be secured urgently to reduce rerupture and clinical worsening. Endovascular coiling is preferable when feasible, but surgical clipping is sometimes needed based on patient or aneurysmal characteristics, or presence of intraparenchymal haemorrhage requiring evacuation. Treatment of symptomatic hydrocephalus with CSF diversion is also crucial. Patients with aneurysmal SAH should be managed by a team of nurses and physicians with neurocritical care, neuroendovascular, and neurosurgical expertise, preferably in a dedicated neurosciences intensive care unit. Early complications include aneurysmal rebleeding, hydrocephalus, and neurogenic cardiopulmonary injury. In the subacute phase, delayed cerebral ischaemia and hyponatremia are more commonly seen. With optimal multidisciplinary management, many patients can return to their previous level of function only weeks after the aneurysm rupture. Still, most treatments in SAH are based on insufficient evidence, and more collaborative research from the bench to the bedside is necessary to continue improving patient outcomes.

Intracerebral haemorrhage and subarachnoid haemorrhage are associated with considerable morbidity and mortality. Too often the focus is on acute treatment after a haemorrhage has occurred, instead of primary and secondary prevention. Medical therapies to control hypertension, achieve tobacco abstinence, and avoid excessive alcohol consumption can confer broad reductions in haemorrhage risk across pathophysiological subtypes. Judicious restriction of antiplatelet and anticoagulant therapies to only those individuals and those intensities for which they are indicated also can substantially reduce haemorrhagic stroke frequency. Specific endovascular and surgical therapies, judiciously employed, will further reduce risk of first or recurrent haemorrhage from structural vascular anomalies, including arteriovenous malformation, cavernous malformations, and saccular aneurysms. For unruptured intracranial aneurysms, features that favour consideration of preventive occlusion include include younger patient age, prior subarachnoid haemorrhage from a different aneurysm, familial intracranial aneurysms, large aneurysm size, irregular shape, basilar or vertebral artery location, and aneurysm growth on serial imaging. Among individuals who are technical candidates for either coiling or clipping, endovascular coiling is associated with a reduction in procedural morbidity and mortality but has a higher risk of recurrence.

For hypertensive patients without prior stroke, TIA, or other symptomatic vascular disease, anti-hypertensive therapy reducing SBP by 10 mm Hg, is associated with reductions in recurrent stroke (by about one-quarter) and of combined stroke, MI, and vascular death (by about one-fifth). Benefit extends across all ages, race-ethnicities, and pathological stroke subtypes. Combined pharmacological and non-pharmacological therapy to lower blood pressure is indicated in all individuals with SBP> 140 or DBP> 90, and in individuals with SBP 130–139 or DBP 80–89 who have additional vascular risk factors. Non-pharmacological blood pressure lowering is indicated in individuals with SBP 130–139 or DBP 80–89 without important additional vascular risk factors. After an ischaemic stroke or TIA, treatment may be gradually started as early as 24–72 hours after onset. The absolute benefits of antihypertensive therapy increase with greater reductions in BP, and are higher for preventing recurrent stroke than for preventing MI, in both primary and secondary prevention. The degree of BP reduction more greatly influences vascular event prevention than does pharmacological agent class. Nonetheless, unless otherwise indicated, beta-blockers are not a preferred agent, as they show less efficacy for stroke prevention. Calcium channel antagonists, ACE inhibitors, and thiazide diuretics are particularly well-studied.

Non-invasive brain stimulation to stimulate neuroplasticity, enhance recovery, and improve mood after stroke has made substantial technical advances in the past two decades. The most common neuromodulatory techniques are transcranial direct current stimulation (tDCS), applying a weak electrical current across the brain, and transcranial magnetic stimulation (TMS), inducing an electrical field within the brain. Currently, the only non-invasive brain stimulation technique and indication for which there is a sufficiently strong evidence base to support routine use in clinical practice is transcranial magnetic stimulation to improve mood in post-stroke depression. TMS applied to dorsolateral prefrontal cortices can substantially reduce depressive symptoms, though not increase complete remission. TMS is a reasonable second-line intervention in patients with post-stroke depressed mood who have been resistant to pharmacotherapy. For several additional indications in post-stroke patients, both TMS and tDCS have shown signals of potential benefit in randomized trials. The strongest evidence is for enhancement of recovery of upper extremity motor function and hand dexterity with TMS. In addition, there is suggestive evidence for possible benefit in improving recovery of function after stroke in walking (TMS), activities of daily living (tDCS), aphasia (both), hemispatial neglect (both), and swallowing (both). However, for these and potentially other recovery-enhancing applications, substantial additional larger trials are needed.

In acute ischaemic stroke, cerebral blood flow autoregulatory mechanisms may be disrupted so that cerebral perfusion becomes reliant on systemic blood pressure. Too low blood pressure may lead to progression of the infarction and too high blood pressure may cause cerebral oedema or haemorrhagic transformation of the infarct. In patients with BP = 220/120 mm Hg who do not receive intravenous thrombolysis, it is reasonable to lower BP by 15% during the first 24 hours after stroke onset. Patients who have elevated blood pressure and are otherwise eligible for treatment with intravenous rt-PA should have their blood pressure lowered so that systolic blood pressure is < 185 mm Hg and their diastolic blood pressure is < 110 mm Hg before thrombolytic treatment is administered. Acute stroke patients should be assessed for dehydration and a fluid balance chart should be kept. Underlying causes of hypotension should be treated rapidly. There is no beneficial effect of hemodilution treatment for acute ischaemic stroke. Fibrinogen-depleting agents that reduce viscosity may marginally reduce risk of recurrent ischaemic stroke, but more greatly increases symptomatic intracranial haemorrhage. Methylxanthine derivatives such as pentoxyphylline and propenofylline that reduce viscosity and produce vasodilation have insufficient evidence to support their use.

Prehospital stroke care is the first link in the stroke chain of survival and includes symptom recognition, engagement of the Emergency Medical Services (EMS) system, timely and effective dispatcher response, and emergency medical response. Prehospital stroke screening tools are an important component in guiding the EMS response to stroke and proper triage of patients. Additionally, there is a growing body of research focused on applications for telemedicine, mobile stroke units, and diagnostic testing in the prehospital arena. Prehospital stroke care is integral to the organization of regionalized stroke systems. Implementation of stroke systems of care can lead to improved access to specialty services and improved patient health outcomes. In addition to increasing access to acute stroke care, telestroke shows great potential for integrating stroke systems of care and facilitating interactions between centres.

Pre-clinical studies provide clear and consistent evidence that a variety of centrally acting drugs affecting specific neurotransmitters can either facilitate or interfere with functional recovery after brain injury. Although at least some clinical trials suggest similar effects in humans, results have been inconsistent. The impact of important factors such as drug dose, duration, and intensity of physiotherapy, and timing between injury and treatment are difficult to translate from preclinical studies. Issues related to variability in stroke severity, location of injury, and comorbid conditions further complicate trial design and could obscure a true treatment effect. Because of these and other issues, the design of efficacy trials assessing putative neuro-restorative interventions is not trivial. Although a proven pharmacological approach resulting in a clinically meaningful improvement in post-stroke recovery remains elusive, it is reasonable to avoid medications that may have harmful effects in patients who have had a stroke. It is also important to control for these possible harmful effects in future clinical trials assessing the outcomes of stroke patients after the acute period.

Although higher plasma cholesterol concentrations have not been reported to be associated with increased stroke risk, cholesterol lowering has been reported to decrease this risk. This decrease can be achieved with statins, which are well-tolerated, provided they are not given to patients with active liver or muscle diseases. Statin treatment in addition to a healthy lifestyle is recommended for the primary prevention of ischaemic stroke in patients with pre-existing coronary heart disease or other high-risk conditions such as diabetes and hypertension. Statins with intensive lipid-lowering effects are recommended for their positive influence on reducing the risks of stroke and cardiovascular events for patients with prior ischaemic stroke or TIA presumed to be of non-cardioembolic origin, even with an LDL-C level =100 mg/dL, with or without evidence of other clinical atherosclerotic cardiovascular diseases. Despite the good safety profile of statins, further studies are clarify safety in patients with prior cerebral haemorrhage and if they may increase brain haemorrhage to a small degree. PCSK9 inhibitors are advised, as add-on therapy to statins, for patients with a high cardiac risk not able to achieve an optimal LDL-C level, though studies with longer follow-up are needed

In the year 2010, an estimated 16.9 million strokes occurred worldwide at an incidence rate of 258 per 100,000 persons per year. Approximately 70% of these strokes occurred in low- and middle-income countries. The 16.9 million incident strokes were added to a pool of 33 million prevalent stroke survivors. There were 5.9 million deaths and 102 million disability-adjusted life-years (DALYs) lost due to stroke in 2010, making stroke the second leading cause of death and the third leading cause of DALYs worldwide. In the preceding two decades, between 1990 and 2010, the incidence rate of stroke remained stable but the absolute number of incident strokes increased by 68%, the prevalence rate increased modestly yet the absolute number of stroke survivors nearly doubled, the rate of DALYs lost due to stroke decreased but the absolute number of DALYs lost increased by 12%, and the mortality rate fell but the absolute number of stroke-related deaths increased by 26%. Most of the burden of stroke is in low-income and middle-income countries, which bear 63% of incident ischaemic strokes and 80% of haemorrhagic strokes. The average age of incident ischaemic and haemorrhagic strokes was 6 years younger in low- and middle– than high–income countries.