IM18.1-16 | Cerebrovascular Accident — Glossary

A practical guideline for timing of anticoagulation initiation after AF-related cardioembolic ischaemic stroke based on stroke severity to minimise haemorrhagic transformation risk: TIA = 1 day; minor stroke (NIHSS <5) = 3 days; moderate stroke (NIHSS 5–15) = 6 days; large stroke (NIHSS >15) = 12 days.

Plasma-derived concentrate of clotting factors II, VII, IX, X, protein C and S; used for emergency reversal of warfarin anticoagulation in ICH; achieves INR reversal within 30–60 minutes; preferred over FFP for speed and lower volume.

A plasma-derived concentrate of factors II, VII, IX, X, and protein C/S; used for rapid reversal of warfarin anticoagulation in life-threatening bleeding (including anticoagulant-related ICH); faster and lower volume than fresh frozen plasma for achieving INR reversal.

A method for estimating haematoma volume on CT: A (largest axial diameter) × B (perpendicular diameter on same slice) × C (number of CT slices with haematoma × slice thickness) ÷ 2; volume >30 mL = 70% 30-day mortality; >60 mL = near-universally fatal without surgery.

A clinical risk stratification tool after TIA: Age ≥60 (1), BP ≥140/90 (1), Clinical features — unilateral weakness (2) or speech disturbance without weakness (1), Duration — ≥60 min (2) or 10–59 min (1), Diabetes (1); score ≥4 indicates high short-term stroke risk requiring urgent inpatient evaluation and dual antiplatelet therapy.

Recombinant tissue plasminogen activator; the standard IV thrombolytic for acute ischaemic stroke; dose 0.9 mg/kg (maximum 90 mg), 10% as IV bolus and 90% as 60-minute infusion; window ≤4.5 hours from last known well.

Supplies the medial surface of the frontal and parietal lobes including the leg area of the motor and sensory cortex; occlusion causes contralateral leg weakness greater than arm weakness and abulia.

A thrombophilic disorder characterised by venous and arterial thrombosis (including stroke) and obstetric morbidity, associated with persistent antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-β2GP1) on two occasions ≥12 weeks apart (Sapporo/Sydney criteria).

An acquired disorder of language — including production, comprehension, repetition, naming, reading, and writing — caused by damage to language areas of the dominant (usually left) cerebral hemisphere; distinct from dysarthria (motor articulation disorder with intact language content).

Tear in the arterial intima allowing blood to track between wall layers, forming an intramural haematoma that narrows the true lumen; the most common cause of ischaemic stroke in adults <45 years; confirmed by crescentic T1 hyperintensity on fat-saturation neck MRI.

Alberta Stroke Programme Early CT Score — a 10-point scoring system for the MCA territory on NCCT brain; starts at 10, subtracts 1 for each of 10 defined regions showing early ischaemic change; ASPECTS ≥6 generally required for mechanical thrombectomy eligibility.

The most common cardiac cause of cardioembolic stroke; thrombus forms in the left atrial appendage due to stagnant blood; annual stroke risk is approximately 5% in untreated AF; anticoagulation decision based on CHA₂DS₂-VASc score.

A large multicentre RCT evaluating very early mobilisation after stroke; found that very early, high-dose mobilisation (first session within 24 hours, multiple daily sessions) was associated with a reduced proportion achieving a favourable outcome compared to usual care early mobilisation; current recommendation: begin mobilisation early (24–48 hours) but avoid ultra-early high-dose protocols.

A GABA-B agonist used as oral antispastic therapy in post-stroke spasticity; dose 5 mg TDS titrated to 20–80 mg/day; side effects include sedation, weakness, and — on abrupt withdrawal — seizures and hallucinations; most effective for generalised spasticity rather than focal spasticity where Botox is preferred.

A neurotoxin that blocks acetylcholine release at the neuromuscular junction, producing temporary (3–4 month) focal muscle paralysis; gold standard for focal post-stroke spasticity (e.g., equinovarus foot, spastic upper limb) where oral antispastic agents have been insufficient; creates a therapeutic window for physiotherapy.

Non-fluent aphasia with preserved comprehension, impaired repetition, and impaired naming; caused by damage to Broca's area (posterior inferior frontal gyrus, left hemisphere); the patient is typically frustrated and aware of the deficit; often associated with right hemiplegia.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; NOTCH3 mutation; presents with migraines, psychiatric symptoms, recurrent lacunar strokes; MRI shows anterior temporal lobe white matter changes; a genetic cause of young stroke.

Deposition of amyloid-beta protein in the walls of cortical and leptomeningeal vessels, causing fragility and predisposition to rupture; the most important cause of lobar intracerebral haemorrhage in elderly patients, often recurrent.

Thrombosis of cerebral venous sinuses causing raised ICP, venous infarction, and haemorrhage; associated with OCP, peripartum state, and hypercoagulable states; diagnosed by MRI+MRV; treated with anticoagulation EVEN when CT shows haemorrhagic infarction.

A rapidly developing episode of focal or global neurological dysfunction lasting more than 24 hours (or leading to death), caused by vascular pathology of the brain; encompasses ischaemic stroke, intracerebral haemorrhage, and subarachnoid haemorrhage.

A clinical prediction score for stroke risk in non-valvular atrial fibrillation: Congestive heart failure (1), Hypertension (1), Age ≥75 (2), Diabetes (1), Stroke/TIA prior (2), Vascular disease (1), Age 65–74 (1), Sex category female (1); score ≥2 in males or ≥3 in females warrants oral anticoagulation.

A small aneurysm formed at the bifurcation of deep perforating arteries in the setting of chronic hypertension; rupture causes hypertensive intracerebral haemorrhage at characteristic sites (putamen, thalamus, pons, cerebellum).

The arterial anastomotic ring at the base of the brain formed by the anterior communicating artery, bilateral posterior communicating arteries, and proximal segments of the ACA, MCA, PCA, and basilar artery; provides collateral flow between anterior and posterior circulations; anatomically complete in only ~20–25% of individuals.

Aphasia characterised by fluent speech, intact comprehension, and markedly impaired repetition; caused by damage to the arcuate fasciculus connecting Broca's and Wernicke's areas through the left parietal lobe.

Both eyes deviated to the same side; in acute hemispheric stroke, the gaze is directed toward the affected hemisphere (away from the hemiplegia) because the frontal eye field drives gaze contralaterally and is destroyed; in pontine lesion, gaze is directed away from the lesion (toward the hemiplegia).

A speech rehabilitation technique paralleling CIMT — the patient is required to use verbal communication even when other modalities (writing, gestures) are available; forces intensive practice of verbal expression; effective for chronic aphasia as well as sub-acute phase.

A rehabilitation technique in which the unaffected limb is constrained (with a mitt or sling) to force use of the affected limb; drives cortical reorganisation in the motor cortex; requires at least some preserved wrist/finger extension to be applicable; most effective in the sub-acute phase (weeks 2–12).

Dynamic CT technique mapping cerebral blood flow (CBF), blood volume (CBV), mean transit time (MTT), and time-to-peak; used to quantify the core-penumbra mismatch — core (CBF severely reduced) versus penumbra (MTT prolonged, CBV preserved) — to guide late-window thrombectomy decisions (DAWN, DEFUSE-3 trials).

Surgical removal of part of the skull to allow the oedematous brain to expand, relieving transtentorial herniation; indicated in malignant MCA infarction (large MCA territory infarct with cerebral oedema) in patients under 60 years; reduces mortality from ~80% to 22% but increases proportion surviving with severe disability (DESTINY, DECIMAL, HAMLET trials).

A transient physiological depression of function in brain areas remote from but connected to a cerebral lesion; explains the initial flaccidity, hyporeflexia, and ipsilateral plantar response seen immediately after a stroke despite the UMN nature of the lesion.

Combination of aspirin (75–300 mg) and clopidogrel (300 mg loading, then 75 mg daily) for 21 days in minor ischaemic stroke (NIHSS ≤3) or high-risk TIA (ABCD2 ≥4); reduces 90-day recurrent stroke by ~25% compared to aspirin alone (POINT and CHANCE trials).

MRI finding where an acute infarct is bright on DWI (restricted diffusion) but not yet bright on FLAIR; indicates infarct age <4.5–6 hours; the basis for the WAKE-UP trial protocol allowing IV thrombolysis in wake-up stroke when the last-known-well time is unknown.

A motor speech disorder causing impaired articulation due to weakness, paralysis, or incoordination of the muscles of speech production; language content (naming, comprehension, repetition) is intact; types: spastic (UMN/corticobulbar), ataxic (cerebellar), flaccid (bulbar/LMN).

A filling defect in the superior sagittal sinus on contrast-enhanced CT, representing sinus thrombus; a diagnostic sign of superior sagittal sinus thrombosis in CVST.

The mechanism of neuronal death in ischaemic core — energy failure leads to massive glutamate release into the extracellular space, which activates NMDA receptors, causing uncontrolled calcium influx into neurons, triggering mitochondrial dysfunction, reactive oxygen species production, and cell death.

Dorsiflexion of the great toe with fanning of the other toes on stroking the lateral sole; indicates an upper motor neuron lesion above the level of the anterior horn cells; persists even in the acute flaccid phase of stroke when other UMN signs may be absent.

A neurosurgical drain placed through a burr hole into the cerebral ventricle to drain CSF and monitor ICP; indicated in obstructive hydrocephalus from intraventricular haemorrhage or large cerebellar ICH compressing the fourth ventricle.

Stroke recognition acronyms: FAST = Face drooping, Arm weakness, Speech difficulty, Time; BEFAST adds Balance and Eyes to improve sensitivity for posterior circulation strokes.

Bladder dysfunction caused by sacral spinal cord or cauda equina lesion: detrusor areflexia with urinary retention and overflow incontinence; associated with LMN lesions — not typical of cerebral stroke.

Severe impairment of all language functions (production, comprehension, repetition, naming); caused by a large left MCA territory infarct destroying both Broca's and Wernicke's areas; typically accompanied by right hemiplegia and right hemianopia.

Conversion of an ischaemic infarct into a haemorrhagic one due to reperfusion injury or the effects of thrombolytic agents; may be petechial (clinically silent) or confluent (symptomatic); the most feared complication of IV thrombolysis, occurring in 3–7% of treated patients.

A neurological syndrome most commonly from right parietal lesions, in which the patient fails to attend to the contralateral (left) visual, auditory, or somatosensory space; causes significant ADL and safety impairment including failure to dress the left side, eat from the left half of the plate, and — critically — detect hazards on the left when driving.

Failure to attend to stimuli on the side contralateral to a brain lesion, typically the left side after right parietal stroke; tested by double simultaneous stimulation; may coexist with anosognosia (unawareness of the deficit) and hemiplegia.

Loss of the same half of the visual field in both eyes (e.g., left half in both left and right eyes); caused by a lesion posterior to the optic chiasm — optic tract, optic radiation, or occipital cortex; the most prominent feature of PCA territory stroke.

Hyperdensity of the proximal MCA on non-contrast CT indicating intraluminal thrombus; sensitivity ~35–50%, specificity ~90%; its presence should trigger CT angiography to confirm and characterise large vessel occlusion.

A specific humanised antibody fragment that reverses dabigatran anticoagulation within minutes; the antidote of choice for life-threatening dabigatran-related bleeding including ICH; dose 5 g IV in two 2.5 g boluses.

The area of densest ischaemia (CBF <10–15 mL/100 g/min) where irreversible neuronal death has already occurred via excitotoxicity; visible on DWI-MRI as restricted diffusion; not salvageable by reperfusion.

Randomised trial demonstrating that intensive BP lowering (target SBP <140 mmHg) within 6 hours of ICH onset was safe and associated with improved functional outcome at 3 months compared to a guideline-recommended BP target of <180 mmHg; established SBP <140 mmHg as the target for ICH.

Spontaneous bleeding into brain parenchyma; the most common cause is hypertensive Charcot-Bouchard microaneurysm rupture; classic sites are putamen (50%), thalamus (15%), cerebellum (10%), and pons (10%); lobar ICH in elderly is associated with cerebral amyloid angiopathy.

The zone of moderate ischaemia (CBF 15–25 mL/100 g/min) surrounding the infarct core; electrically silent but metabolically viable; potentially salvageable if perfusion is restored within the therapeutic window (4.5 hours for thrombolysis, up to 24 hours for mechanical thrombectomy with penumbra imaging).

A small spherical infarct (≤15 mm diameter) in the deep perforating artery territory (basal ganglia, internal capsule, thalamus, pons) caused by lipohyalinosis of a single perforating artery; produces one of five classic lacunar syndromes without cortical features.

The time at which the patient was last observed to be at their neurological baseline; the starting point of the thrombolysis clock — not the time symptoms were noticed. For wake-up strokes, LKW is the time the patient went to sleep.

Hyaline thickening and narrowing of the walls of small perforating arteries driven by chronic hypertension and diabetes; the underlying vessel pathology of lacunar infarction.

A state produced by bilateral basilar artery occlusion causing pontine infarction: the patient has intact consciousness (reticular activating system spared) but complete paralysis of all voluntary movement except vertical eye movements and blinking (corticospinal and corticobulbar tracts destroyed in the pons).

A hyperosmolar agent used in acute management of raised intracranial pressure in stroke; 20% solution 0.5–1 g/kg IV over 15–20 minutes; draws free water from brain parenchyma by osmotic gradient; monitor for hypotension and electrolyte disturbances.

Endovascular removal of an occluding thrombus from a proximal cerebral artery (ICA, M1 MCA, basilar) using a stent retriever or aspiration catheter under fluoroscopic guidance; indicated within 6 hours of onset for proximal LVO (up to 24 hours with favourable penumbra-core mismatch in DAWN/DEFUSE-3 trial-eligible patients).

The largest branch of the internal carotid artery; supplies the lateral surface of the frontal, parietal, and temporal lobes including primary motor cortex (arm/face), Broca's area, Wernicke's area, and the internal capsule via lenticulostriate branches; occlusion causes contralateral hemiplegia (arm > leg), hemisensory loss, and aphasia (dominant hemisphere).

A 0–6 scale of functional disability used in stroke medicine: 0=no symptoms; 1=no significant disability; 2=slight disability (independent but unable to carry out all previous activities); 3=moderate disability (requires some help but walks independently); 4=moderately severe (unable to walk, unable to attend to own body needs); 5=severe disability; 6=death. Premorbid mRS is an eligibility factor for thrombolysis.

The brain's capacity for structural and functional reorganisation after injury; the biological basis of stroke recovery; includes cortical remapping, synaptic sprouting, and recruitment of ipsilateral pathways; maximally active in the first 3–6 months post-stroke and is use-dependent — driven by repetitive, task-specific practice.

A validated 11-domain neurological assessment tool scoring consciousness, gaze, vision, facial palsy, arm motor, leg motor, limb ataxia, sensory, language, dysarthria, and extinction; range 0–42; scores ≤4 = minor, 5–15 = moderate, 16–20 = moderate-severe, ≥21 = severe.

A calcium channel blocker given orally (60 mg every 4 hours for 21 days) after subarachnoid haemorrhage; reduces cerebral vasospasm (a major cause of delayed ischaemic neurological deficit after SAH); does not prevent vasospasm but reduces its clinical consequences.

A rehabilitation discipline focused on restoring functional independence in activities of daily living (ADLs) — dressing, bathing, cooking, writing; provides adaptive equipment, home modification recommendations, and driving assessments; particularly important for upper limb impairment, hemispatial neglect, and return to work planning.

An error in language production in which an incorrect word is substituted; phonemic paraphasia = substitution of a word with a phonetically similar word ('tork' for 'fork'); semantic paraphasia = substitution of a word from the same category ('spoon' for 'fork'); neologism = a made-up word.

A persistent opening between the right and left atria through the remnant of the foetal foramen ovale; found in ~25–30% of the population and ~40–50% of young cryptogenic stroke; paradoxical embolism (venous thrombus crossing to systemic circulation) is the proposed mechanism.

The clinical practice of allowing elevated blood pressure (up to 220/120 mmHg) in the first 24–48 hours of acute ischaemic stroke without thrombolysis, to maintain perfusion pressure to the ischaemic penumbra; aggressive BP lowering in this phase can extend the infarct.

The Patient Health Questionnaire-9; a validated 9-item self-reported depression screening tool; score 0–4 = minimal, 5–9 = mild, 10–14 = moderate, 15–19 = moderately severe, 20–27 = severe depression; used routinely at every post-stroke review to detect post-stroke depression early.

Depression occurring after stroke, affecting 30–35% of survivors; driven by direct brain injury, psychosocial adjustment, and biochemical changes; a major predictor of poor rehabilitation outcome; screened with PHQ-9; treated with SSRI (escitalopram preferred) and psychological support.

Epilepsy arising after stroke; early seizures (within 7 days) occur in approximately 5% of stroke patients and do not predict late epilepsy; late seizures (after 7 days) predict epilepsy risk of 3–5%; routine prophylactic antiepileptics are NOT recommended in the absence of seizures; patients should be counselled and should not drive until seizure-free for the legally required period.

Supplies the occipital lobe, inferomedial temporal lobe, and thalamus via thalamoperforating branches; occlusion causes contralateral homonymous hemianopia with macular sparing.

A sensitive test for mild corticospinal tract lesion: with arms held outstretched and palms up, eyes closed, the affected arm pronates and drifts downward; may be present even when gross strength testing appears normal.

A 2019 randomised controlled trial (Lancet) addressing whether to restart antiplatelet therapy after intracranial haemorrhage; found that restarting antiplatelets (mainly aspirin) reduced recurrent major vascular events without significantly increasing recurrent ICH; supports resuming antiplatelets in most patients with a separate vascular indication after 4–8 weeks post-ICH.

A structured communication framework for delivering difficult news: Setting (private, family present), Perception (what does the patient/family already understand?), Invitation (does the patient want detailed information?), Knowledge (deliver information in steps without jargon), Empathy (acknowledge and name the emotion), Summary (summarise the plan and next steps).

Active contrast extravasation into the haematoma on CTA, indicating ongoing bleeding and haematoma expansion in ICH; associated with early neurological deterioration and high 30-day mortality.

Bleeding into the subarachnoid space; the classic cause is rupture of an intracranial saccular ('berry') aneurysm at the bifurcations of the Circle of Willis; presents with sudden-onset 'thunderclap headache' — worst headache of the patient's life.

A large vessel granulomatous vasculitis affecting the aorta and major branches (including carotid and vertebral origins); predominantly young Asian women; can cause stroke by carotid/vertebral stenosis or occlusion; elevated ESR; CTA/MRA shows wall thickening and stenosis.

A genetically engineered tPA variant with greater fibrin specificity and longer half-life; given as a single IV bolus at 0.25 mg/kg (maximum 25 mg); increasingly preferred when mechanical thrombectomy is planned due to simplicity of administration.

The time period within which IV thrombolysis is potentially effective for acute ischaemic stroke: standard window ≤4.5 hours from last known well for alteplase and tenecteplase; beyond 4.5 hours, haemorrhagic transformation risk outweighs benefit for most patients.

A panel of blood tests to identify hypercoagulable states in young stroke: protein C, protein S, antithrombin III, activated protein C resistance (factor V Leiden), prothrombin G20210A, homocysteine, and antiphospholipid antibody panel.

Trial of Org 10172 in Acute Stroke Treatment classification of ischaemic stroke by mechanism: large artery atherosclerosis, cardioembolism, small vessel occlusion (lacunar), stroke of other determined aetiology, and cryptogenic.

A transient episode of focal neurological dysfunction without infarction on DWI-MRI; historically defined as resolving within 24 hours; risk of stroke after TIA is 10–15% within 48 hours without treatment — a medical emergency.

Echocardiography using an oesophageal probe; superior to TTE for detecting left atrial appendage thrombus, PFO (bubble contrast study), and aortic arch plaques; essential in young cryptogenic stroke workup.

Bladder dysfunction caused by suprasacral UMN lesion (as in most strokes): the sacral detrusor reflex is intact but cortical inhibition is lost, resulting in urge incontinence and urinary frequency; the most common bladder pattern after stroke.

Weakness predominantly affecting the lower face (nasolabial fold flattening, drooping corner of mouth) with forehead sparing, because the frontalis receives bilateral cortical input and is relatively spared by unilateral hemispheric lesions; localises the lesion to the contralateral hemisphere.

The gold standard investigation for post-stroke dysphagia; real-time fluoroscopic visualisation of swallowing with barium contrast, characterising the phase of dysfunction (oral, pharyngeal, oesophageal) and degree of aspiration; guides dietary texture modification and swallowing technique.

A posterior fossa stroke syndrome from PICA occlusion causing lateral medullary infarction; characterised by ipsilateral facial numbness, contralateral body numbness (spinothalamic), ipsilateral Horner syndrome, ipsilateral limb ataxia, dysphagia, dysarthria, and hoarseness.

A brainstem (midbrain) crossed syndrome: ipsilateral CN III palsy (ptosis, dilated pupil, 'down and out' eye) + contralateral hemiplegia; caused by an infarct in the midbrain cerebral peduncle.

Fluent aphasia with severely impaired comprehension, paraphasias, and impaired repetition; caused by damage to Wernicke's area (posterior superior temporal gyrus, left hemisphere); the patient is often unaware of the errors (anosognosia); often without hemiplegia.

Yellow discolouration of the CSF supernatant after centrifugation, due to bilirubin from oxyhaemoglobin breakdown; appears 2–4 hours after SAH onset, persists up to 2 weeks; distinguishes true SAH from a traumatic lumbar puncture.