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Stroke

Original Editor - Wendy Walker Top Contributors - Admin, Wendy Walker, Kim Jackson, Rachael Lowe, Laura Ritchie, Vidya Acharya, Stacy Schiurring, Naomi O'Reilly, Lucinda hampton, Katherine McBeth, Jess Bell, Tony Lowe, Scott Buxton, Sweta Christian, Priyanka Chugh, Simisola Ajeyalemi, Magdalena Hytros, Evan Thomas, Karen Wilson, Rucha Gadgil, Amrita Patro and 127.0.0.1

Defining Stroke

At its core, a stroke represents a failure of the brain's blood supply. A stroke occurs when the blood supply to an area of the brain is disrupted, depriving neural tissue of the oxygen and glucose it needs to survive. Understanding what that means in practice, and how it unfolds clinically, requires more than a single-sentence definition.


Under the ICD-11, which came into effect in January 2022, stroke is defined as an acute episode of focal or global cerebral, spinal, or retinal dysfunction caused by infarction or haemorrhage in the central nervous system.[1] This definition marks a meaningful departure from earlier classifications: it no longer requires symptoms to persist for 24 hours. Instead, it incorporates imaging-confirmed tissue injury as a diagnostic criterion, even when symptoms resolve more quickly. This change has real clinical implications, as it reclassifies some presentations previously labelled as transient ischaemic attack (TIA) into the stroke category when neuroimaging confirms tissue damage.[2]

There are two main classifications of stroke: ischaemic and haemorrhagic.

Ischaemic Stroke

Ischaemic stroke accounts for approximately 85% of all strokes. It occurs when a blood vessel supplying the brain becomes blocked, either by a clot forming locally (thrombosis) or by material travelling from elsewhere in the body and lodging in a cerebral vessel (embolism). A third mechanism, systemic hypoperfusion, occurs when a global reduction in blood pressure or cardiac output (caused by events such as cardiac arrest, severe haemorrhage, sepsis, or major surgery) overwhelms the brain's ability to maintain stable blood flow through its normal autoregulatory mechanisms. The regions most vulnerable are the watershed zones, which sit at the furthest margins between adjacent arterial territories. They are the first to be deprived when perfusion pressure drops. This produces a characteristic pattern of injury, most visible as proximal limb weakness, with the shoulders and hips more affected than the hands and feet. Unlike thrombotic or embolic stroke, the cause is systemic rather than localised, which has direct implications for how the patient's broader medical history is understood and how rehabilitation is approached.[3]

The TOAST classification identifies five ischaemic subtypes.[4] The three most relevant to rehabilitation professionals are large artery atherosclerosis, cardioembolic stroke and small vessel occlusion (lacunar stroke). In large artery atherosclerosis, plaque build-up in major vessels causes thrombosis or distal embolisation. Cardioembolic stroke, most commonly from atrial fibrillation, accounts for up to 20–30% of ischaemic strokes. It typically produces more severe presentations and requires anticoagulation rather than antiplatelet therapy.[5] In small vessel occlusion (lacunar stroke), small penetrating arteries are occluded by hypertensive or diabetic vessel wall changes, producing small deep infarcts that spare cortical function.

Haemorrhagic Stroke

Haemorrhagic stroke accounts for approximately 15% of all strokes but carries a disproportionately high burden of early mortality and disability. Its two subtypes differ substantially in cause, presentation, and rehabilitation implications and are best understood as distinct clinical entities.

Intracerebral haemorrhage (ICH) occurs when a blood vessel ruptures directly within the brain parenchyma. Chronic hypertension is the most common cause. The typical presentation is sudden focal neurological deficits that progress over minutes to hours as the haematoma expands, with reduced consciousness common in larger bleeds. Thirty-day mortality ranges from 34–50%, and approximately half of survivors remain dependent for activities of daily living.[6]

For rehabilitation professionals, timing of mobilisation is an important distinction from ischaemic stroke: rehabilitation activities such as stretching and functional task training may be considered 24–48 hours after moderate ICH, but early aggressive mobilisation within the first 24 hours appears to worsen 14-day mortality.[6] Early motor gains should not be mistaken for full recovery. Cognitive screening, blood pressure monitoring, and attention to recurrent ICH risk are vital throughout rehabilitation.[7]

Subarachnoid haemorrhage (SAH) occurs when bleeding enters the subarachnoid space. In approximately 80% of cases, the cause is rupture of an intracranial aneurysm. The hallmark presentation is a sudden, severe headache (frequently described as the worst headache of the patient's life), accompanied by nausea, vomiting, photophobia, and neck stiffness. Any presentation fitting this description should be treated as a medical emergency regardless of setting.

Among survivors, the rehabilitation burden of SAH is frequently underestimated. Physical, cognitive, behavioural, and quality of life deficits are common and can persist well beyond apparent physical recovery. Fatigue, mood disturbance, and cognitive difficulties (particularly memory, processing speed, and executive function) can profoundly affect return to work and daily function.[8]

The Vascular Supply of the Brain

Understanding where strokes occur and what deficits they produce begins with the brain's vascular architecture. At the base of the brain sits a ring of communicating arteries known as the Circle of Willis, the central junction of the brain's blood supply and the structure from which the major cerebral arteries arise.[9]

The circle is formed by contributions from two sources. Anteriorly, the two internal carotid arteries enter and give rise to the anterior cerebral arteries and middle cerebral arteries. Posteriorly, the two vertebral arteries join at the pontomedullary junction to form the basilar artery, which bifurcates terminally into the posterior cerebral arteries. These anterior and posterior systems are connected by communicating vessels: the anterior communicating artery bridges the two anterior cerebral arteries across the midline, and the two posterior communicating arteries link the internal carotid system to the posterior cerebral arteries on each side.[9] It is this arrangement that gives the Circle of Willis its potential as a collateral pathway, an alternative route that blood can take if a primary vessel becomes occluded. This helps to preserve perfusion to tissue that would otherwise be at risk.

The Major Cerebral Arterial Territories

Three pairs of major cerebral arteries arise from the Circle of Willis: (1) the anterior cerebral arteries, (2) the middle cerebral arteries, and (3) the posterior cerebral arteries. The vertebrobasilar system supplies the brainstem and cerebellum. Each territory supplies specific brain regions with distinct functions; knowing the vascular territory involved gives a strong clinical prediction of the deficits your patient is likely to present with.

The table below provides an overview of each arterial territory, the structures supplied, and the key functions at risk.[10][11][12][13]

Artery Structures Supplied Key Functions at Risk
Middle Cerebral Artery (MCA)
  • Lateral frontal, parietal, temporal lobes
  • Internal capsule
  • Basal ganglia
  • Motor
  • Sensation
  • Language
  • Spatial awareness
Anterior Cerebral Artery (ACA)
  • Medial frontal and parietal lobes
  • Anterior corpus callosum
  • Lower limb motor/sensory
  • Movement initiation
  • Bladder control
Posterior Cerebral Artery (PCA)
  • Occipital lobe
  • Hippocampus
  • Thalamus
  • Midbrain
  • Vision
  • Memory
  • Face recognition
  • Sensory relay
Vertebrobasilar System
  • Brainstem
  • Cerebellum
  • Inner ear
  • Coordination
  • Cranial nerves III–XII
  • Swallowing
  • Consciousness

Stroke Clinical Presentations

Middle Cerebral Artery (MCA)

Middle Cerebral Artery (MCA) strokes account for approximately 70% of all ischaemic strokes.[14] The MCA's extensive territory means that a stroke here rarely produces a single, isolated deficit. Instead, it generates a complex combination of motor, sensory, communicative, and perceptual impairments. Lenticulostriate branches supply the tightly packed corticospinal tract in the internal capsule, where small infarcts produce disproportionate motor impairment.[10] MCA strokes characteristically produce contralateral hemiparesis with the arm and face more affected than the leg, contralateral sensory loss, homonymous hemianopia, and conjugate gaze deviation towards the lesion side.[10][15]

The clinical picture differs depending on which hemisphere is affected, and these differences are substantial enough that left and right MCA presentations are best understood separately.[15]

Left MCA stroke Right MCA stroke
Typical Presentation
  • Contralateral (right-sided) hemiparesis: the arm and face are more affected than the leg
  • Contralateral sensory loss: right arm and face
  • Contralateral homonymous hemianopia: right visual field loss
  • Conjugate gaze deviation towards the left (side of lesion)
  • Aphasia: expressive (Broca's), receptive (Wernicke's), or mixed depending on extent of involvement; the patient may understand well, but struggle to produce words, or speak fluently but with impaired comprehension
  • Reading, writing, and calculation difficulties with larger infarcts
  • Motor and sensory deficits without the perceptual and attentional features typical of right hemisphere involvement
  • Contralateral (left-sided) hemiparesis: the arm and face are more affected than the leg
  • Contralateral sensory loss: left arm and face
  • Contralateral homonymous hemianopia: left visual field loss
  • Conjugate gaze deviation towards the right (side of lesion)
  • Left hemispatial neglect (occurs in up to 45% of right hemisphere strokes in the acute phase)
  • Anosognosia (present in approximately 81% of patients with hemispatial neglect)
  • Constructional apraxia
  • Impaired prosody
  • Language typically preserved, but communication is affected by perceptual and attentional deficits
Anterior Cerebral Artery (ACA)

Anterior Cerebral Artery (ACA) strokes account for 0.3–4.4% of ischaemic strokes.[11] Because the paracentral lobule rather than the lateral motor strip is at risk, deficits are the inverse of MCA stroke: contralateral lower limb weakness and sensory loss more pronounced than upper limb, with bladder incontinence from medial cortical involvement. The frontal lobe involvement produces a set of neurobehavioural changes that are clinically important and frequently misinterpreted. Patients with ACA strokes typically present with motor problems, mutism, delayed initiation, reduced fluency, apathy, and overall frontal lobe dysfunction.[16] Abulia (meaning reduced initiative, motivation, and spontaneity) from anterior cingulate and medial frontal involvement is prominent[11] and frequently misread as low mood or poor rehabilitation potential. The patient is not refusing to participate; their brain is struggling to initiate. Strategies reducing initiation demands, such as environmental cues and structured routines, can be remarkably effective. A grasp reflex and other frontal release signs may be present, and some patients develop gait apraxia (meaning difficulty initiating walking despite having adequate motor strength).[11]

Posterior Cerebral Artery (PCA)

Posterior Cerebral Artery (PCA) strokes account for 5–10% of ischaemic strokes. Motor function is often relatively preserved, risking underestimation of the clinical picture. Contralateral homonymous hemianopia occurs in approximately 84% of cases; recovery is often limited, significantly affecting driving, reading, and navigation. Visual agnosia (meaning the inability to recognise objects despite intact visual acuity) and prosopagnosia (meaning the inability to recognise familiar faces, typically from right PCA involvement) carry profound safety implications. When thalamic structures are involved, contralateral hemisensory loss and central post-stroke pain may develop, sometimes only emerging weeks to months after onset. Memory impairment from hippocampal involvement, and movement disorders including tremor or dystonia may also develop.[12]

Vertebrobasilar System (Posterior Circulation)

Vertebrobasilar system strokes account for 20–25% of ischaemic strokes and are frequently underdiagnosed. The brainstem's compact architecture means small infarcts produce wide-ranging deficits. The key clinical signal is crossed findings: ipsilateral cranial nerve deficits paired with contralateral motor or sensory changes in the body (i.e. facial findings on one side with limb findings on the other).

Wallenberg syndrome (also known as lateral medullary syndrome) is the most common posterior circulation syndrome. It results from lateral medullary infarction, typically from PICA or vertebral artery occlusion. It produces ipsilateral facial pain and temperature loss with contralateral body pain and temperature loss, ipsilateral Horner syndrome, ipsilateral ataxia, vertigo, nystagmus, dysphagia, dysarthria, and hoarseness. Persistent hiccups are diagnostically useful.[17]

Cerebellar infarction produces characteristic ipsilateral findings: limb ataxia with dysmetria and intention tremor, truncal ataxia affecting sitting and standing balance, and a wide-based unsteady gait. Nystagmus, dysarthria, vertigo, headache, and neck pain are common. Large cerebellar infarctions carry a risk of herniation from cerebellar oedema and represent a potential neurosurgical emergency.[18]

Basilar artery occlusion is a neurological emergency at the most severe end of the posterior circulation spectrum.[19] It can result in locked-in syndrome – a state in which the patient is fully conscious but has complete paralysis of all voluntary movement except vertical eye movements, which become their only means of communication. Rehabilitation professionals should be aware of this condition as they may encounter patients in the subacute phase.[20]

Pontine strokes can produce pure motor weakness, dysarthria, ataxia, or combinations of these, with cranial nerve involvement causing ipsilateral facial weakness, hearing loss, or eye movement abnormalities depending on the level of the lesion.[21]

Less Common Types of Stroke

A working knowledge of less common types of stroke is important for rehabilitation professionals, both because they are encountered in practice, and because their presentations are easy to miss or misattribute.

Lacunar Strokes

Lacunar strokes are small deep infarcts less than 15 mm. They are caused by small vessel occlusion in the internal capsule, basal ganglia, thalamus, or pons. They account for 20–25% of ischaemic strokes. The absence of cortical signs (i.e. no aphasia, neglect, or visual field deficits) is a distinguishing feature.[22]

Patients present with one of four classic syndromes.

  1. Pure motor hemiparesis. Equal weakness of face, arm, and leg; no sensory or cognitive involvement; typically internal capsule or pons.
  2. Pure sensory stroke. Hemisensory loss without weakness; typically thalamic.
  3. Ataxic hemiparesis. Ipsilateral weakness combined with ataxia on the same side; typically posterior internal capsule or pons.
  4. Sensorimotor stroke. Combined motor and sensory deficits; typically thalamocapsular.

Early recovery can be deceptively encouraging. Cerebral small vessel disease is the most common cause of vascular cognitive impairment, with features extending beyond cognition to include impaired balance, falls, depression, and apathy.[22] Cognitive screening from the outset is essential.

Spinal Cord Infarction

Spinal cord infarction accounts for 1–2% of vascular neurological presentations and is frequently misdiagnosed as musculoskeletal pathology.[23] Anterior spinal artery occlusion produces bilateral motor weakness below the lesion, with bladder and bowel dysfunction. There is also dissociated sensory loss: pain and temperature are lost while proprioception and vibration are preserved.[24] Sudden severe back or neck pain typically precedes the neurological deficit. Preserved proprioception is a genuine rehabilitation asset that can be leveraged in balance and movement work even when motor recovery is incomplete.

Cerebral Venous Sinus Thrombosis

Cerebral venous sinus thrombosis (CVST) causes stroke through impaired venous drainage rather than arterial occlusion. It accounts for 0.5–3% of strokes and most commonly affects young adults, women of reproductive age, and those with prothrombotic conditions.[25] The most common presenting symptom is a severe progressive headache developing over days, distinct from the instantaneous onset of SAH. Seizures are more frequent than in arterial stroke. Deficits do not follow a clear arterial territory pattern, so this diagnosis is easily missed. When a patient's demographic profile does not fit typical arterial stroke, CVST should remain in the differential.

Retinal Artery Occlusion

Retinal artery occlusion presents as sudden, painless, monocular vision loss and is classified as a stroke equivalent under the ICD-11. Approximately 30% of patients with acute central retinal artery occlusion present with concurrent cerebral ischaemia on MRI,[26] and subsequent stroke risk is significantly elevated.[27] For rehabilitation professionals working in any setting, sudden monocular vision loss is a medical emergency. Do not continue the session. Activate emergency services immediately.

Resources

Clinical Resources:
Clinical Guidelines:

References

  1. ↑ Feigin VL, Brainin M, Norrving B, Martins SO, Pandian J, Lindsay P, F Grupper M, Rautalin I. World stroke organization: global stroke fact sheet 2025. International Journal of Stroke. 2025 Feb;20(2):132-44.
  2. ↑ Groff H, Yousfani S, Pantoja-Ruiz C, Douiri A, Bhalla A, Wolfe C, Marshall IJ. A systematic review of the incidence and outcomes of ICD-11 defined stroke. Journal of Stroke and Cerebrovascular Diseases. 2024 Aug 1;33(8):107784.
  3. ↑ Momjian-Mayor I, Baron JC. The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies. Stroke. 2005 Mar 1;36(3):567-77.
  4. ↑ Adams Jr HP, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh 3rd EE. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. stroke. 1993 Jan;24(1):35-41.
  5. ↑ Chao TF, Potpara TS, Lip GY. Atrial fibrillation: stroke prevention. The Lancet Regional Health–Europe. 2024 Feb 1;37.
  6. ↑ 6.0 6.1 Greenberg SM, Ziai WC, Cordonnier C, Dowlatshahi D, Francis B, Goldstein JN, Hemphill III JC, Johnson R, Keigher KM, Mack WJ, Mocco J. 2022 guideline for the management of patients with spontaneous intracerebral hemorrhage: a guideline from the American Heart Association/American Stroke Association. Stroke. 2022 Jul;53(7):e282-361.
  7. ↑ Matchett SC, Castaldo J, Wasser TE, Baker K, Mathiesen C, Rodgers J. Predicting mortality after intracerebral hemorrhage: comparison of scoring systems and influence of withdrawal of care. Journal of Stroke and Cerebrovascular Diseases. 2006 Jul 8;15(4):144-50.
  8. ↑ Nwafor DC, Kirby BD, Ralston JD, Colantonio MA, Ibekwe E, Lucke-Wold B. Neurocognitive sequelae and rehabilitation after subarachnoid hemorrhage: optimizing outcomes. Journal of vascular diseases. 2023 Apr 1;2(2):197-211.
  9. ↑ 9.0 9.1 Rosner J, Reddy V, Lui F. Neuroanatomy, Circle of Willis [Internet]. 2023 [cited 27 May 2026]. Available from:https://www.ncbi.nlm.nih.gov/books/NBK534861/?report=reader
  10. ↑ 10.0 10.1 10.2 Margetis K, Sánchez-Manso JC. Neuroanatomy, Middle Cerebral Artery [Internet]. 2025 [cited 27 May 2026]. Available from:https://www.ncbi.nlm.nih.gov/books/NBK526002/?report=reader
  11. ↑ 11.0 11.1 11.2 11.3 Matos Casano HA, Tadi P, Ciofoaia GA. Anterior Cerebral Artery Stroke [Internet]. 2023 [cited 27 May 2026]. Available from:https://www.ncbi.nlm.nih.gov/books/NBK537333/?report=reader
  12. ↑ 12.0 12.1 Benjamin R, Tadi P, Singh J. Posterior Cerebral Artery Stroke [Internet]. 2026 [cited 27 May 2026]. Available from:https://www.ncbi.nlm.nih.gov/books/NBK532296/?report=reader
  13. ↑ Piccinin MA, Munakomi S. Neuroanatomy, Vertebrobasilar System [Internet]. 2023 [cited 27 May 2026]. Available from:https://www.ncbi.nlm.nih.gov/sites/books/NBK540995/
  14. ↑ TadiP, Lui F. Posterior Acute Stroke [Internet]. 2023 [cited 27 May 2026]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK535369/
  15. ↑ 15.0 15.1 Benjamin R, Galuska MA. Middle Cerebral Artery Stroke [Internet]. 2026 [cited 29 May 2026]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556132/
  16. ↑ Cruces R, Muñoz-García I, Palmer-Cancel SJ, Salas C. A Neuropsychological Rehabilitation Framework to Address Cognitive and Neurobehavioral Impairments After Strokes to the Anterior Communicating Artery. Frontiers in Human Neuroscience. 2022 Jun 10;16:808011.
  17. ↑ National Institute of Neurological Disorders and Stroke. Lateral Medullary Syndrome. Available from: https://www.ninds.nih.gov/health-information/disorders/lateral-medullary-syndrome [Accessed 29 May 2026].
  18. ↑ Lui F, Naqvi IA. Cerebellar Infarction [Internet]. 2026 [cited 27 May 2026]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470416/
  19. ↑ Lui F, Hegazy MI. Basilar Artery Occlusion [Internet]. 2026 [cited 30 May 2026]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532241/
  20. ↑ Zelik U, Florczak W, Śnieżna J, Dziewic J, Dzwonnik K, Domino W, Trestka G, Przygoda M, Włodyka J, Stępień K, Adamczyk S. Locked-in Syndrome: Insights into Etiology, Diagnosis, Management, and Quality of Life. Quality in Sport. 2025 Jan 22;37:57097-.
  21. ↑ Malla G, Jillella DV. Pontine Infarction [Internet]. 2023 [cited 30 May 2026]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554418/
  22. ↑ 22.0 22.1 Markus HS, de Leeuw FE. Cerebral small vessel disease: recent advances and future directions. International Journal of Stroke. 2023 Jan;18(1):4-14.
  23. ↑ Althobaiti F, Maghrabi R, Alharbi N, Alwadai M, Almatrafi MK, Bajammal S. Anterior spinal artery syndrome in a patient with multilevel cervical disc disease: A case report. Cureus. 2024 Jul 15;16(7).
  24. ↑ Sandoval JI, De Jesus O. Anterior Spinal Artery Syndrome [Internet]. 2024 [cited 30 May 2026]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560731/
  25. ↑ Saposnik G, Bushnell C, Coutinho JM, Field TS, Furie KL, Galadanci N, Kam W, Kirkham FC, McNair ND, Singhal AB, Thijs V. Diagnosis and management of cerebral venous thrombosis: a scientific statement from the American Heart Association. Stroke. 2024 Mar;55(3):e77-90.
  26. ↑ Al Jarallah O. Risk of acute stroke in patients with retinal artery occlusion: a systematic review and meta-analysis. European Review for Medical & Pharmacological Sciences. 2023 Jun 15;27(12).
  27. ↑ Wai KM, Knapp A, Ludwig CA, Koo E, Parikh R, Rahimy E, Mruthyunjaya P. Risk of stroke, myocardial infarction, and death after retinal artery occlusion. JAMA ophthalmology. 2023 Dec;141(12):1110-6.
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