Cerebrovascular & Stroke

Epidemiology

Incidence

aSAH is a minority of all strokes but accounts for a disproportionate share of stroke-related years of life lost, given the relatively young age of many patients.

Age peak

Commonly middle age; key risk factors are hypertension and smoking.

Location

Aneurysms cluster at bifurcations of the circle of Willis (e.g. anterior communicating, posterior communicating, and middle cerebral artery bifurcation).

Clinical Presentation

• A sudden, severe 'thunderclap' headache, classically described as 'the worst headache of my life', with or without transient loss of consciousness, neck stiffness, photophobia, or a focal deficit.
• Clinical severity is graded (Hunt and Hess; World Federation of Neurosurgical Societies, WFNS) and the blood burden on CT is graded (Fisher / modified Fisher) to estimate the risk of delayed vasospasm.

Imaging

• Non-contrast CT is the first investigation and is highly sensitive within the first hours. If CT is negative but the history is convincing, lumbar puncture (xanthochromia) or CT angiography is used.
• CT angiography and/or digital subtraction angiography (DSA) define the aneurysm and the vascular anatomy for treatment planning.

Management

Surgery. The ruptured aneurysm is secured early to prevent re-bleeding, by endovascular coiling or microsurgical clipping. In the ISAT trial of ruptured aneurysms judged suitable for both, endovascular coiling gave better survival free of disability at 1 year (dependency or death 23.7% vs 30.6% with clipping); aneurysm characteristics, patient age, and local expertise guide the choice in a neurovascular team.

Adjuvant therapy. Oral nimodipine is given routinely and improves outcome after aSAH (in the British aneurysm nimodipine trial it reduced cerebral infarction and poor outcome). Delayed cerebral ischaemia from vasospasm is actively monitored and treated, and acute hydrocephalus may require CSF diversion with an external ventricular drain.

Considerations. Care follows contemporary AHA/ASA guidance and is best delivered in a high-volume neurovascular and neurocritical-care setting.

Outcomes

aSAH carries substantial early mortality and long-term morbidity; early aneurysm securing, nimodipine, and management of delayed cerebral ischaemia and hydrocephalus improve outcomes.

By molecular subgroup: Higher clinical grade (Hunt–Hess / WFNS) and a greater blood burden (modified Fisher) predict worse outcome and a higher vasospasm risk.

Epidemiology

Incidence

Present in a small percentage of the adult population, frequently found incidentally.

Age peak

Adults; risk factors include hypertension, smoking, and a family history of aneurysms or SAH.

Location

Anterior circulation is most common; posterior-circulation and posterior-communicating aneurysms carry a higher rupture risk.

Clinical Presentation

• Usually asymptomatic and incidental. Larger aneurysms may cause mass effect; a posterior-communicating aneurysm, for instance, can produce a painful third-nerve palsy.
• A new symptomatic aneurysm (e.g. a fresh cranial-nerve palsy or sentinel headache) warrants urgent assessment.

Imaging

• CT angiography or MR angiography characterises size, location, and morphology; digital subtraction angiography is used when finer detail is needed for treatment planning.
• Surveillance imaging is used for aneurysms managed conservatively.

Management

Surgery. Treatment (endovascular or microsurgical) is considered for higher-risk aneurysms, while many small, low-risk aneurysms are monitored. In ISUIA, the 5-year rupture risk rose with size and posterior location, and the procedural risk could equal or exceed the natural-history risk for small anterior lesions.

Adjuvant therapy. The PHASES score aggregates Population, Hypertension, Age, Size of aneurysm, earlier SAH, and Site to estimate 5-year rupture risk and support shared decision-making.

Considerations. Modifiable risk factors, above all hypertension and smoking, are addressed in every patient, whether or not the aneurysm is treated.

Outcomes

Most small, anterior, incidentally found aneurysms have a low annual rupture risk; the decision to treat is individualised.

By molecular subgroup: Larger size, posterior-circulation / posterior-communicating location, prior SAH, hypertension, and older age increase rupture risk (captured by the PHASES score).

Epidemiology

Incidence

Uncommon, but a notable cause of haemorrhagic stroke in younger adults.

Age peak

Often present in young and middle-aged adults.

Location

Supratentorial in the majority.

Clinical Presentation

• Haemorrhage (the most feared presentation), seizures, focal deficit, or headache; some are incidental.
• Presentation with rupture substantially raises the priority for treatment to prevent re-haemorrhage.

Imaging

• MRI/MR angiography and CT/CT angiography show the nidus and draining veins; digital subtraction angiography (DSA) is the gold standard for defining angioarchitecture and planning treatment.

Management

Surgery. Treatment options are microsurgical resection, endovascular embolisation, and stereotactic radiosurgery — used alone or in combination. The Spetzler–Martin grade (nidus size, eloquence of adjacent brain, and pattern of venous drainage) stratifies surgical risk and guides selection.

Adjuvant therapy. For unruptured AVMs specifically, the ARUBA trial found medical management alone superior to intervention for the composite of death or symptomatic stroke over the trial follow-up. The decision to treat an unruptured AVM should therefore be cautious and individualised.

Considerations. Ruptured AVMs are generally treated to prevent re-haemorrhage; unruptured AVM management is individualised within a multidisciplinary neurovascular team in light of ARUBA.

Outcomes

Outcome depends on presentation (ruptured vs unruptured), angioarchitecture and Spetzler–Martin grade, and the treatment chosen.

By molecular subgroup: Higher Spetzler–Martin grades carry greater surgical morbidity; for unruptured AVMs, intervention caused more strokes and deficits than medical management in ARUBA.

Epidemiology

Incidence

Accounts for a substantial share of strokes and a disproportionate share of stroke mortality.

Age peak

Risk rises with age; deep ICH relates to hypertension, and lobar ICH in the elderly to cerebral amyloid angiopathy.

Location

Deep (basal ganglia, thalamus, pons, cerebellum) versus lobar.

Clinical Presentation

• Acute focal deficit with headache and reduced consciousness; deterioration may follow haematoma expansion.
• Level of consciousness, haematoma volume, and intraventricular extension are key prognostic features.

Imaging

• Non-contrast CT confirms and localises the haemorrhage and allows volume estimation (e.g. the ABC/2 method); CT angiography may show a 'spot sign' or an underlying vascular lesion.
• Vascular imaging is considered to exclude an underlying aneurysm, AVM, or tumour, particularly in lobar or otherwise atypical haemorrhage.

Management

Surgery. Management is primarily medical (blood-pressure control, reversal of anticoagulation, neurocritical care). Routine early surgery for supratentorial ICH has not shown overall benefit: STICH found no overall advantage of early surgery over initial conservative treatment, and STICH II showed that early surgery for superficial lobar ICH without intraventricular haemorrhage did not improve the primary outcome (with at most a small survival signal).

Adjuvant therapy. A few situations are exceptions. Cerebellar haemorrhage with brainstem compression or hydrocephalus is generally evacuated, and external ventricular drainage is used for hydrocephalus or intraventricular extension. Care follows AHA/ASA guidance.

Considerations. Decisions weigh haematoma location and size, the neurological trajectory, and patient factors, within a neurocritical-care pathway.

Outcomes

ICH carries high mortality and major disability; outcome depends on haematoma volume and location, level of consciousness, and intraventricular extension.

By molecular subgroup: Routine surgical evacuation of supratentorial ICH has not improved outcomes in trials; cerebellar haemorrhage with compression is a recognised surgical indication.

Epidemiology

Incidence

A common cause of ischaemic stroke and transient ischaemic attack.

Age peak

Older adults with vascular risk factors.

Location

Carotid bifurcation and the origin of the internal carotid artery.

Clinical Presentation

• Often detected after an ipsilateral transient ischaemic attack (including transient monocular blindness) or a non-disabling stroke; some stenoses are asymptomatic.
• Symptomatic status and the degree of stenosis drive management decisions.

Imaging

• Duplex ultrasound, CT or MR angiography, and (selectively) catheter angiography quantify the stenosis and characterise the plaque.
• The recency of symptoms and the percentage stenosis determine the urgency and choice of revascularisation.

Management

Surgery. Carotid endarterectomy (CEA) markedly reduces stroke in symptomatic high-grade (70–99%) stenosis. In NASCET, the 2-year ipsilateral-stroke risk fell from 26% with medical therapy to 9% with surgery. Best medical therapy (antiplatelet, statin, and risk-factor control) is given to all patients.

Adjuvant therapy. Carotid-artery stenting (CAS) is an alternative to CEA: in CREST the composite of stroke, myocardial infarction, or death did not differ significantly between CAS and CEA, but peri-procedural stroke was higher with stenting and myocardial infarction higher with endarterectomy, and this informs the patient-specific choice.

Considerations. Revascularisation is most beneficial soon after a symptomatic event and is individualised by age, anatomy, and comorbidity, always combined with optimal medical therapy.

Outcomes

Revascularisation plus medical therapy reduces stroke in symptomatic high-grade carotid stenosis; benefit is greatest with higher degrees of stenosis and prompt treatment after symptoms.

By molecular subgroup: CEA and CAS give similar long-term composite outcomes (CREST); peri-procedural stroke favours CEA, and lower myocardial-infarction risk favours CAS.