Stroke (Overview)

Article Last Updated:09/06/2026

Stroke

A stroke is clinically defined as a syndrome of presumed vascular origin, characterised by rapidly developing signs of focal or global disturbance of cerebral functions that last for more than 24 hours or lead to death. It may be caused by ischaemia, due to interruption of blood supply, or haemorrhage, due to intracranial bleeding.

Content note: The background sections on stroke classification, vascular territories and localising clinical features are based largely on established neuroanatomy, traditional clinical teaching and standard textbook descriptions. They are therefore not extensively referenced to individual sources.

Types of Stroke

Strokes can be categorised into 2 major types, based on their underlying mechanism:

Type	Underlying mechanism	Notes
Ischaemic stroke	Interruption of cerebral blood flow → ischaemia → tissue necrosis There are 2 main mechanisms causing the interruption: Cardioembolic (20-30% cases): clot that forms in the heart and travels to the brain Thrombotic: mainly from atherosclerosis	Most common type of stroke, accounting for ~85% of cases
Haemorrhagic stroke	Blood vessel rupture → non-traumatic intracranial bleeding → brain injury from compression and/or direct tissue damage	Accounts for ~15% of strokes. Main subtypes include: Intracerebral haemorrhage (~10%) Subarachnoid haemorrhage

Type

Underlying mechanism

Notes

Ischaemic stroke

Interruption of cerebral blood flow → ischaemia → tissue necrosis

There are 2 main mechanisms causing the interruption:

Cardioembolic (20-30% cases): clot that forms in the heart and travels to the brain
Thrombotic: mainly from atherosclerosis

Most common type of stroke, accounting for ~85% of cases

Haemorrhagic stroke

Blood vessel rupture → non-traumatic intracranial bleeding → brain injury from compression and/or direct tissue damage

Accounts for ~15% of strokes. Main subtypes include:

Intracerebral haemorrhage (~10%)
Subarachnoid haemorrhage

If the acute loss of cerebral function (i.e. the neurological deficit) resolves completely within 24 hours, it is classified as a transient ischaemic attack (TIA), instead of a stroke.

Note on TIA definition:

Traditional teaching and UK guidance, including NICE, NICE CKS and the UK National Clinical Guideline for Stroke 2023, define stroke and TIA using the 24-hour clinical cut-off
However, some modern definitions, particularly from the AHA/ASA, use a tissue-based definition
- Under this definition, TIA refers to a transient focal neurological deficit caused by ischaemia without evidence of acute infarction
- Therefore, if symptoms fully resolve but imaging shows acute infarction, the event is classified as an ischaemic stroke rather than a TIA

This is included because one may encounter both definitions in clinical practice and in different guideline sources.

Causes and Risk Factors

Shared risk factors:

Hypertension – major modifiable risk factor for both ischaemic stroke and intracerebral haemorrhage
OSA
Lifestyle factors
- Smoking
- Excessive alcohol use
- Physical inactivity

Type-specific causes and risk factors:

Ischaemic stroke	Haemorrhagic stroke
Cardioembolic ischaemic stroke risk factors: Atrial fibrillation – leading cause Mitral valve disease Mechanical heart valves Heart failure Recent MI PFO, ASD, VSD These can cause a paradoxical embolism from the venous system E.g. a DVT thrombus can pass through the defect into the arterial circulation and embolise to the brain, causing an ischaemic stroke rather than a PE Non-cardioembolic ischaemic stroke risk factors: Large vessel disease Carotid artery stenosis Intracranial artery atherosclerosis Cervical artery dissection Prothrombotic conditions (e.g. APS) Metabolic conditions (e.g. hypercholesterolaemia, obesity, insulin resistance) COCP and HRT use	Primarily driven by: ^[Ref] Arteriosclerosis – strongly associated with hypertension, diabetes and old age Cerebral amyloid angiopathy – associated with older age Other causes and risk factors: Anticoagulant or antiplatelet use Macrovascular abnormalities AVMs Intracranial aneurysms Dural fistulas Cavernous malformation

Ischaemic stroke

Haemorrhagic stroke

Cardioembolic ischaemic stroke risk factors:

Atrial fibrillation – leading cause
Mitral valve disease
Mechanical heart valves
Heart failure
Recent MI
PFO, ASD, VSD
- These can cause a paradoxical embolism from the venous system
- E.g. a DVT thrombus can pass through the defect into the arterial circulation and embolise to the brain, causing an ischaemic stroke rather than a PE

Non-cardioembolic ischaemic stroke risk factors:

Large vessel disease
- Carotid artery stenosis
- Intracranial artery atherosclerosis
- Cervical artery dissection
Prothrombotic conditions (e.g. APS)
Metabolic conditions (e.g. hypercholesterolaemia, obesity, insulin resistance)
COCP and HRT use

Primarily driven by: ^[Ref]

Arteriosclerosis – strongly associated with hypertension, diabetes and old age
Cerebral amyloid angiopathy – associated with older age

Other causes and risk factors:

Anticoagulant or antiplatelet use
Macrovascular abnormalities
- AVMs
- Intracranial aneurysms
- Dural fistulas
- Cavernous malformation

Clinical Features – Shared / Overview

Stroke typically presents with sudden-onset focal neurological symptoms (motor and/or sensory).

Any sudden onset of focal neurological symptoms that persist = stroke until proven otherwise

These patients should be admitted directly and transferred to a hyperacute stroke unit or service ASAP

BE FAST is a useful mnemonic for non-specific stroke features:

Letter	Meaning	Symptoms
B	Balance	Loss of balance / dizziness / vertigo / ataxia
E	Eyes	Visual loss / visual field defect / diplopia
F	Face	Facial drooping / asymmetry
A	Arm	Unilateral arm weakness and/or abnormal sensation
S	Speech	Slurred speech / dysphagia / aphasia
T	Time	Time-critical emergency requiring urgent assessment

Clinical Features – Ischaemic vs Haemorrhagic Stroke

Ischaemic stroke	Haemorrhagic stroke
Classically presents with: Sudden onset Typically painless Neurological deficits	May present similarly to ischaemic stroke but is more likely to be associated with features of mass effect and/or raised ICP Headache Vomiting Seizures Reduced consciousness Severe haemorrhage may cause signs of raised ICP or brainstem compression, such as abnormal pupils, Cushing reflex or coma. A sudden severe thunderclap headache should raise suspicion for subarachnoid haemorrhage.

Ischaemic stroke

Haemorrhagic stroke

Classically presents with:

Sudden onset
Typically painless
Neurological deficits

May present similarly to ischaemic stroke but is more likely to be associated with features of mass effect and/or raised ICP

Headache
Vomiting
Seizures
Reduced consciousness

Severe haemorrhage may cause signs of raised ICP or brainstem compression, such as abnormal pupils, Cushing reflex or coma.

A sudden severe thunderclap headache should raise suspicion for subarachnoid haemorrhage.

Clinical Features – Localising Findings

Note: These localising patterns are most useful for ischaemic stroke, where symptoms often map to a vascular territory. Haemorrhagic stroke may also cause focal deficits, but symptoms are additionally influenced by haematoma size, mass effect, raised ICP and intraventricular extension.

Clinical features of stroke often reflect the affected vessel and vascular territory. Ischaemic stroke can be broadly localised using the Oxford/Bamford classification. ^[Ref]

Subgroup	Description	Clinical features
Total anterior circulation infarct (TACI)	Large anterior circulation infarct, involving MCA and/or ACA artery. Both cortical and subcortical structures are affected.	ALL 3 of the following: Unilateral motor and/or sensory deficit affecting face, arm, and leg (at least 2 body parts) Homonymous hemianopia Higher cerebral dysfunction (e.g. dysphasia / aphasia, neglect, dyspraxia) If there is impaired consciousness, higher cerebral dysfunction and visual field defects are assumed
Partial anterior circulation infarct (PACI)	A less severe anterior circulation infarct, with primarily cortical involvement	2 out of 3 components of TACI (see above), or Isolated higher cerebral dysfunction
Posterior circulation infarct (POCI)	Vertebrobasilar arterial territory involvement, including the brainstem, cerebellum, occipital lobes and/or thalamus	At least one of the following: Visual field defect Brainstem signs Cerebellar signs
Lacunar infarct (LACI)	Small deep infarct affecting perforating (lenticulostriate) arterial territories, commonly involving the internal capsule, basal ganglia, thalamus or pons	Characterised by the absence of cortical signs (= absence of higher cerebral dysfunction and visual field defect) Typical syndromes include: Pure motor stroke Pure sensory stroke Sensorimotor stroke Ataxic hemiparesis Dysarthria-clumsy hand syndrome

Anterior Circulation Stroke

Anterior circulation strokes involve the carotid arterial system, including the internal carotid artery (ICA) and its major branches: the middle cerebral artery (MCA) and anterior cerebral artery (ACA).

Artery / territory	Main affected regions	Typical clinical features
Middle cerebral artery (MCA)	Lateral frontal, parietal and temporal lobes	Contralateral motor and/or sensory loss Weakness affects face and UL > LL Contralateral homonymous hemianopia Dominant hemisphere: dysphasia / aphasia, dyspraxia, Gerstmann-type features Non-dominant hemisphere: neglect, visuospatial dysfunction Note on hemisphere vs hand dominance The dominant hemisphere is the hemisphere primarily responsible for language. In most people, this is the left hemisphere. However, right-sided or bilateral language dominance is more common in left-handed individuals than in right-handed individuals. Clinically, the presence of dysphasia / aphasia usually suggests dominant hemisphere involvement, most commonly a left MCA stroke. Note that hand dominance is not a perfect predictor of language dominance.
Anterior cerebral artery (ACA)	Medial frontal and parietal lobes	Contralateral motor and/or sensory loss Weakness affects LL > face and UL Other possible features: Behavioural / personality changes Apathy / abulia Gait disturbances Urinary incontinence
Ophthalmic / retinal artery	Retina / optic nerve	Sudden painless monocular visual loss

Artery / territory

Main affected regions

Typical clinical features

Middle cerebral artery (MCA)

Lateral frontal, parietal and temporal lobes

Contralateral motor and/or sensory loss

Weakness affects face and UL > LL
Contralateral homonymous hemianopia
Dominant hemisphere: dysphasia / aphasia, dyspraxia, Gerstmann-type features
Non-dominant hemisphere: neglect, visuospatial dysfunction

Note on hemisphere vs hand dominance

The dominant hemisphere is the hemisphere primarily responsible for language.

In most people, this is the left hemisphere.

However, right-sided or bilateral language dominance is more common in left-handed individuals than in right-handed individuals.

Clinically, the presence of dysphasia / aphasia usually suggests dominant hemisphere involvement, most commonly a left MCA stroke. Note that hand dominance is not a perfect predictor of language dominance.

Anterior cerebral artery (ACA)

Medial frontal and parietal lobes

Contralateral motor and/or sensory loss
Weakness affects LL > face and UL

Other possible features:

Behavioural / personality changes
Apathy / abulia
Gait disturbances
Urinary incontinence

Ophthalmic / retinal artery

Retina / optic nerve

Sudden painless monocular visual loss

Posterior Circulation Stroke

Posterior circulation strokes can be harder to recognise than anterior circulation strokes because they may present with non-specific clinical features, often overlapping with other conditions.

Territory / structure	Main affected regions	Typical clinical features
Posterior cerebral artery (PCA)	Occipital lobe, medial / inferior temporal lobe, thalamus	Contralateral homonymous hemianopia with macular sparing Cortical blindness (if there is bilateral PCA involvement) If temporal lobe is involved → memory impairment If thalamus is involved → sensory symptoms or altered consciousness
Cerebellum	Cerebellar hemispheres and vermis	Ipsilateral clinical features (DANISH): Dysdiadochokinesia Ataxia Nystagmus Intention tremor Slurred “scanning” speech Hypotonia

Territory / structure

Main affected regions

Typical clinical features

Posterior cerebral artery (PCA)

Occipital lobe, medial / inferior temporal lobe, thalamus

Contralateral homonymous hemianopia with macular sparing
Cortical blindness (if there is bilateral PCA involvement)
If temporal lobe is involved → memory impairment
If thalamus is involved → sensory symptoms or altered consciousness

Cerebellum

Cerebellar hemispheres and vermis

Ipsilateral clinical features (DANISH):

Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred “scanning” speech
Hypotonia

Brainstem strokes may cause a combination of cranial nerve signs and long-tract signs (e.g. corticospinal, spinothalamic tract involvement), giving the classic crossed signs

Ipsilateral cranial nerve signs, with
Contralateral limb sensory and/or motor deficits

Specific brainstem stroke syndromes:

Syndrome	Affected artery	Affected structures and clinical features
Lateral medullary syndrome (PICA stroke)	Posterior inferior cerebellar artery (PICA)	Tracts: Sympathetic fibres → ipsilateral Horner syndrome Lateral spinothalamic tract → contralateral pain / temperature sensory loss of the body Inferior cerebellar peduncle → ipsilateral ataxia Cranial nerve nuclei: Spinal trigeminal nucleus → ipsilateral facial pain / temperature sensory loss Vestibular nuclei → vertigo, nystagmus, N&V Nucleus ambiguus → dysphagia, dysarthria, hoarseness, ↓ gag reflex
Lateral pontine syndrome (AICA stroke)	Anterior inferior cerebellar artery (AICA)	Tracts: Sympathetic fibres → ipsilateral Horner syndrome Lateral spinothalamic tract → contralateral pain / temperature sensory loss of the body Cerebellar peduncle → ipsilateral ataxia (limb and gait) Cranial nerve nuclei: Spinal trigeminal nucleus → ipsilateral facial pain / temperature sensory loss Facial nerve nuclei → ipsilateral facial weakness (lower motor neuron lesion) Vestibulocochlear nerve nuclei → Vertigo, nystagmus, N&V Hearing loss, tinnitus
Weber syndrome (midbrain stroke)	Paramedian branches of PCA	CN III fibres → ipsilateral CN III palsy Ptosis Fixed, dilated pupil (→ asymmetrical pupil) “Down and out” eye Diplopia Corticospinal tract (cerebral peduncle) → contralateral limb weakness
Locked-in syndrome	Basilar artery	Usually affects the ventral pons: Bilateral corticospinal tracts → quadriplegia Bilateral corticobulbar tracts → anarthria and facial / tongue / pharyngeal weakness The following functions are typically spared: Wakefulness and consciousness (due to RAS sparing) Vertical gaze Blinking

Lacunar Infarct / Stroke

A lacunar infarct is a small, deep ischaemic stroke caused by occlusion of small perforating arteries (lenticulostriate arteries), which supply deep brain structures like:

Internal capsule
Basal ganglia
Thalamus

Lacunar infarct is primarily caused by lipohyalinosis, most commonly due to chronic hypertension and diabetes

Lacunar infarcts are characterised by the absence of cortical signs:

Higher cerebral dysfunction (e.g. dysphasia / aphasia, dyspraxia, neglect)

Key lacunar stroke syndromes:

Syndrome	Typical clinical features
Pure motor stroke (most common)	Most commonly affects the internal capsule (posterior limb) Contralateral weakness affecting face, arm and/or leg
Pure sensory stroke	Most commonly affects the thalamus Contralateral sensory loss
Sensorimotor stroke	Contralateral weakness and sensory loss
Ataxic hemiparesis	Contralateral weakness with ipsilateral limb ataxia/incoordination
Dysarthria-clumsy hand syndrome	Dysarthria with contralateral hand weakness

If a younger patient presents with a lacunar stroke, one should consider CADASIL syndrome – the most common single-gene disorder causing stroke.

Stroke Mimics / Differential Diagnoses

Stroke mimic	Suggestive clinical features
Hypoglycaemia	Capillary blood glucose should be checked urgently in all suspected stroke presentations because hypoglycaemia is an immediately reversible mimic Altered consciousness Sweating Tremor Confusion Tachycardia Seizures / focal neurological deficits
Seizure	Todd’s paresis: post-ictal weakness persisting after the seizure Post-ictal confusion or drowsiness
Migraine	Migraine with aura can cause gradual spread of symptoms over minutes Positive symptoms: visual disturbances (e.g. zigzag lines, sparklets), paraesthesia (often starting in the fingers and travelling up the arm) Negative symptoms: visual field defects, aphasia, numbness Hemiplegic migraine can cause transient unilateral weakness
Functional neurological disorder (conversion disorder)	Neurological symptoms that are inconsistent, fluctuate, or do not follow a typical anatomical pattern. Examination may show signs such as variable weakness or inconsistency between observed function and formal testing.
Bell’s palsy	Isolated lower motor neurone facial weakness affecting both the forehead and lower face. Other clinical features of Bell’s palsy: Hyperacusis (from stapedius muscle involvement) Altered taste on the anterior 2/3 of the tongue (from chorda tympani involvement) Dry eye or excessive tearing Pain around ear / mastoid discomfort Presence of ANY of the following is suggestive of a stroke (or other causes), instead of Bell’s palsy: Facial sensory loss (facial weakness only) Limb weakness and sensory loss Dysphasia Neglect Visual field defect
Vestibular neuritis / labyrinthitis	Acute vertigo, nausea, vomiting and gait unsteadiness without focal neurological signs. Hearing loss or tinnitus suggests labyrinthitis. See the Vestibular Neuronitis and Labyrinthitis article for more information.
Subdural haematoma	Older age, anticoagulant use with recent head injury or falls. Symptoms may be gradual or fluctuating, with headache, confusion, drowsiness or focal neurological deficits. See the Subdural Haemorrhage (SDH) article for more information.
Brain tumour	Progressive neurological symptoms, headache, seizures, personality change, cognitive decline or features of raised intracranial pressure. See the Brain Tumours in Adults article for more information.
Delirium	Acute confusion, reduced attention, fluctuating consciousness. May worsen pre-existing neurological deficits. Common triggers include dehydration, constipation, and infection.
Syncope / pre-syncope	Brief loss of consciousness, light-headedness, pallor, sweating, rapid recovery and absence of persistent focal neurological deficit. May be triggered by standing, dehydration, pain or arrhythmia.

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