Stroke Syndromes Reference

Anterior Circulation

3 syndromes

MCA + ACA (ICA occlusion) 17% of ischaemic strokes

Clinical Features

All 3 required: (1) contralateral hemiparesis ± hemisensory loss, (2) homonymous hemianopia, (3) higher cortical dysfunction (dysphasia if dominant / neglect if non-dominant)

Red Flags & Complications

⚠ Malignant MCA oedema (peak 48–72h) — consider decompressive hemicraniectomy if age <60

⚠ Haemorrhagic transformation — highest risk with large infarct volume + reperfusion

⚠ High aspiration risk — formal swallow assessment mandatory before oral intake

Prognosis

Worst prognosis of OCSP subtypes

~60% 1-year mortality. Only 4% functionally independent at 1 year (Bamford 1991). NIHSS typically >15. If thrombolysed/thrombectomised early, outcomes improve substantially (HERMES: NNT 2.6 for ≥1 mRS level improvement).

Expected mRS: 4–6

MCA branch 34% of ischaemic strokes

Clinical Features

2 of 3 TACI criteria, OR isolated higher cortical dysfunction, OR restricted motor/sensory deficit (e.g. monoparesis)

Superior division: face + arm > leg weakness, Broca's aphasia (dominant), contralateral gaze preference

Inferior division: Wernicke's aphasia (dominant), contralateral hemianopia/quadrantanopia, neglect (non-dominant)

Red Flags

⚠ Highest early recurrence rate (~17% at 1 year)

⚠ Inferior division strokes may present without weakness — often misdiagnosed

Prognosis

Moderate prognosis; high recurrence risk

~16% 1-year mortality. Functional independence at 1 year ~55%.

Expected mRS: 1–4

ACA (A2 segment)

Clinical Features

Contralateral leg > arm weakness (motor strip topography)

Abulia / akinetic mutism (bilateral ACA or dominant mesial frontal)

Urinary incontinence (superior frontal involvement)

Prognosis

Generally better than MCA syndromes

Leg weakness can be prolonged but functional arm use is preserved.

Expected mRS: 1–3

Posterior Circulation

3 syndromes

Vertebrobasilar system 24% of ischaemic strokes

Clinical Features

Ipsilateral CN palsy + contralateral motor/sensory deficit, OR bilateral deficits, OR conjugate gaze disorder, OR cerebellar dysfunction, OR isolated hemianopia

Red Flags

⚠ 39% are FAST-negative — high miss rate in ED

⚠ NIHSS systematically underscores posterior circulation deficits

⚠ Basilar occlusion can present with fluctuating symptoms → catastrophic deterioration

Prognosis

Best early functional outcome; highest late recurrence

~19% 1-year mortality. Best functional independence (~62%). However, 20% late recurrence at 5 years.

Expected mRS: 0–3

PICA / vertebral artery

Clinical Features

Ipsilateral: facial numbness (V), Horner's, cerebellar ataxia, hoarseness/dysphagia (IX/X)

Contralateral: spinothalamic sensory loss (pain/temp)

Lateropulsion (falling toward lesion), vertigo, nystagmus

Key absence: NO limb weakness (corticospinal tract spared)

Red Flags

⚠ Severe dysphagia — aspiration risk; NGT often required

⚠ May present as acute vertigo → misdiagnosed as vestibular neuritis. Use HINTS exam

Prognosis

Generally good motor prognosis

Most recover well functionally (mRS 0–2). Dysphagia resolves in ~2/3. Central pain (Déjerine-Roussy) can develop and be debilitating.

Expected mRS: 0–2

Basilar artery (ventral pons)

Clinical Features

Quadriplegia (bilateral corticospinal tracts)

Bilateral facial + bulbar paralysis

Anarthria, aphagia

PRESERVED: consciousness, vertical eye movements, blinking

Red Flags

⚠ MUST be distinguished from coma — patient is fully aware

⚠ EEG shows normal waking patterns (confirms awareness)

⚠ Risk of being inappropriately treated as GCS 3 → premature withdrawal of care

Prognosis

Devastating but not uniformly fatal

Historical 1-year mortality ~60–70%. ~10% achieve partial motor recovery. Long-term survivors report higher quality of life than expected.

Expected mRS: 5 (typically)

Cerebellar Strokes

Vascular territories · HINTS · Surgical indications

Arterial Supply — Quick Reference

PICA

Inferior cerebellum + lateral medulla

← Vertebral artery · Most common cerebellar infarct

AICA

Anteroinferior cerebellum + lateral pons

← Basilar artery (lower) · Least common

SCA

Superior cerebellum + dorsolateral midbrain

← Basilar artery (upper) · Most prominent ataxia

⚡ Key Differentiators

PICA — dysphagia + Wallenberg features (Horner's, crossed sensory loss, lateropulsion)

AICA — unilateral hearing loss + ipsilateral LMN facial weakness (unique to AICA)

SCA — severe ipsilateral limb ataxia + intention tremor, most prominent dysarthria

All three — vertigo, gait ataxia, dysarthria, nystagmus

Key absence — NO limb weakness (unless brainstem compression)

Inferior cerebellum + lateral medulla Most common cerebellar infarct

Core Features

Vertigo, nausea, vomiting (vestibular nuclei)

Ipsilateral limb ataxia (cerebellar hemisphere)

Gait ataxia / truncal instability — may not sit unsupported

Dysarthria (cerebellar)

Nystagmus (direction-changing or gaze-evoked)

Occipital headache (often prominent)

+ Wallenberg (if lateral medulla involved)

Ipsilateral facial pain/numbness (CN V — descending tract)

Ipsilateral Horner's syndrome (ptosis, miosis, anhidrosis)

Ipsilateral palatal/vocal cord paralysis (CN IX/X) → dysphagia, hoarseness, reduced gag

Contralateral spinothalamic loss (pain/temp) — body & limbs

Lateropulsion (falling toward lesion side)

Key absence: NO limb weakness (corticospinal tract spared)

Red Flags

⚠ Large PICA infarct → cerebellar swelling peaks 48–72h → posterior fossa emergency

⚠ Dysphagia from medullary involvement → aspiration risk — NBM until assessed

⚠ Vertebral artery dissection common in younger patients — CTA/MRA

Prognosis

Generally good if no brainstem compression

Isolated cerebellar infarcts: most achieve mRS 0–2. Vertigo and ataxia improve over weeks–months. Wallenberg component: dysphagia resolves in ~2/3; central neuropathic pain can be chronic. Gait ataxia is often the last deficit to recover.

mRS 0–2 (isolated) / 2–4 (with medullary involvement)

Anteroinferior cerebellum + lateral pons Least common; unique auditory involvement

Core Features

Vertigo, nausea, vomiting

Ipsilateral hearing loss — sudden, unilateral (labyrinthine artery is AICA branch)

Tinnitus (ipsilateral)

Ipsilateral LMN facial weakness (CN VII — lateral pons)

Ipsilateral limb ataxia

Ipsilateral facial numbness (CN V)

Ipsilateral Horner's syndrome

Contralateral spinothalamic loss (pain/temp)

Ipsilateral gaze palsy (CN VI — lateral pons)

Red Flags

⚠ Acute vertigo + unilateral deafness = AICA territory until proven otherwise — NOT labyrinthitis

⚠ Labyrinthine artery branches from AICA → isolated sudden hearing loss can herald impending AICA infarction

⚠ Ipsilateral LMN facial palsy may mimic Bell's palsy if cerebellar signs are subtle

⚠ Basilar branch disease — may indicate broader posterior circulation compromise

Prognosis

Moderate; hearing loss often permanent

Cerebellar and vestibular symptoms generally recover well. Hearing loss from labyrinthine artery involvement is usually permanent (end-artery, no collateral supply). Facial weakness recovers variably. Extensive pontine involvement worsens prognosis.

Expected mRS: 1–3

Superior cerebellum + dorsolateral midbrain Most prominent limb ataxia

Core Features

Ipsilateral limb ataxia — often severe, arm + leg (superior cerebellar peduncle)

Dysarthria (cerebellar — often prominent)

Gait ataxia

Intention tremor / dysmetria (dentate nucleus involvement)

Ipsilateral Horner's syndrome

Contralateral spinothalamic loss (pain/temp) — if lateral midbrain involved

Contralateral CN IV palsy (superior oblique) — if midbrain involved

Nystagmus

Red Flags

⚠ SCA territory swelling → upward transtentorial herniation (cerebellum pushes up through tentorial notch)

⚠ Superior cerebellar peduncle carries major efferent output — severe ipsilateral ataxia, slow to recover

⚠ Bilateral SCA infarcts (basilar tip embolism) → severe pancerebellar syndrome ± midbrain signs

Prognosis

Good functional outcome; ataxia can be prolonged

Most achieve independence (mRS 0–2). Limb ataxia is the most prominent and persistent deficit — may take months to plateau. Dysarthria usually improves. Midbrain involvement adds motor/sensory deficits and worsens trajectory. Intention tremor can be disabling even with otherwise good recovery.

mRS 0–2 (isolated) / 2–4 (with midbrain involvement)

Cerebellar hemisphere (SCA branches) Most treatable ICH subtype

Core Features

Acute severe occipital headache

Nausea/vomiting — often severe and persistent

Ipsilateral limb ataxia

Gait ataxia / inability to walk

Dysarthria

NO limb weakness initially — new weakness = brainstem compression

Ipsilateral gaze palsy / CN VI palsy

Red Flags — NEUROSURGICAL EMERGENCY

⚠ Posterior fossa is a confined space → rapid deterioration possible — patient can go alert → comatose within minutes

⚠ Surgical evacuation: haematoma ≥3cm diameter OR declining GCS OR hydrocephalus (AHA/ASA 2022 Class I)

⚠ Obstructive hydrocephalus: 4th ventricle compression → urgent EVD

⚠ Both upward transtentorial AND tonsillar herniation possible — both lethal

⚠ New limb weakness or decerebrate posturing = brainstem compression → immediate neurosurgery, do not wait for imaging

Prognosis

Bimodal: excellent with early surgery; devastating without

The most surgically treatable ICH subtype. Early suboccipital decompression/evacuation → mRS 0–2 (among best outcomes of any ICH). Without surgery, brainstem compression is often fatal. Small haematomas (<3cm) without hydrocephalus or brainstem compression can be managed conservatively with close monitoring.

mRS 0–2 (post-surgery) / 5–6 (untreated compression)

HINTS Exam

Distinguishing central from peripheral acute vestibular syndrome · >95% sensitive for stroke (superior to early MRI in first 24–48h)

Head Impulse Test

Rapid passive head rotation — observe for corrective saccade

Peripheral (reassuring): Positive — corrective saccade present (vestibular nerve not generating VOR)

Central (concerning): Negative — normal VOR, no saccade (brainstem/cerebellum is the problem)

💡 Normal HIT in acute vertigo = DANGEROUS (central cause)

Nystagmus

Observe in primary gaze and with lateral gaze

Peripheral: Unidirectional, horizontal, suppressed by fixation

Central: Direction-changing with gaze direction, vertical, or torsional — not suppressed by fixation

💡 Direction-changing nystagmus = central

Test of Skew

Alternating cover test — observe for vertical refixation

Peripheral: No skew deviation

Central: Vertical skew deviation (one eye higher) — brainstem vestibular pathway dysfunction

💡 Any skew = central until proven otherwise

⚠ Interpretation

If ANY single feature is central-pattern → treat as central (stroke) and image urgently. All three must be peripheral-pattern to confidently diagnose peripheral vestibulopathy.

Remember: MRI-DWI can be FALSE NEGATIVE for posterior fossa infarcts in first 24–48h — HINTS outperforms early MRI.

Surgical Decision-Making

Cerebellar stroke with mass effect — AHA/ASA 2022

Haematoma ≥3cm diameter (ICH)

Urgent

Declining GCS (any cerebellar stroke)

Emergency

Obstructive hydrocephalus (4th ventricle compression)

Emergency

Large cerebellar infarct with oedema (peak 48–72h)

Urgent

Brainstem compression (new weakness, posturing, pupil changes)

Emergency

✓ Conservative criteria

Small haematoma (<3cm) or infarct without hydrocephalus, mass effect, or brainstem compression → close neuro-obs (q1h GCS + pupils), repeat CT at 6h (ICH) or 24–48h (infarct), HOB 30°, BP management per guidelines, neurosurgical standby.

📋 Monitoring Checklist

GCS and pupil checks q1h (minimum) — escalate immediately if any decline

Repeat CT: 6h (ICH) or 24–48h (infarct), or immediately if clinical change

HOB elevated 30° to reduce ICP

Strict BP management (ICH: SBP <140 within 1h per AHA/ASA 2022)

NBM until formal swallow assessment

Inform neurosurgery early — even if conservative initially

Have EVD kit available on ward/ICU

Lacunar Syndromes

5 syndromes

Internal capsule / pons 25% of all strokes

Clinical Features

Contralateral face, arm, and leg weakness (proportional)

No sensory loss, visual field deficit, or cortical dysfunction

Prognosis

Best prognosis of lacunar syndromes

~75% achieve functional independence. Motor recovery often substantial over 3–6 months.

Expected mRS: 0–2

VPL thalamic nucleus

Clinical Features

Contralateral numbness / paraesthesiae (face, arm, leg)

All modalities affected (touch, pinprick, proprioception, vibration)

No motor deficit, no cortical signs

Red Flags

⚠ Thalamic pain syndrome (Déjerine-Roussy) can develop weeks–months later

Prognosis

Good functional prognosis; neuropathic pain risk

Most patients return to independence. 8–16% develop chronic thalamic pain syndrome.

Expected mRS: 0–1

Haemorrhagic Stroke

6 types

Lenticulostriate arteries

Clinical Features

Contralateral hemiparesis + hemisensory loss

Homonymous hemianopia

Global aphasia (dominant) / neglect (non-dominant)

Ipsilateral gaze deviation ('eyes look toward lesion')

Red Flags

⚠ Haematoma expansion in first 24h (~38%) — repeat CT at 6h

⚠ IVH extension → acute hydrocephalus

⚠ Midline shift > 5mm → consider surgical evacuation

Prognosis

Variable; volume-dependent (ICH Score)

Small ICH (<30mL) with preserved consciousness has reasonable recovery. INTERACT2: intensive BP lowering (SBP <140) improves outcomes.

Expected mRS: 2–6

Superior cerebellar artery

Clinical Features

Acute severe headache, nausea/vomiting

Ipsilateral limb ataxia / gait ataxia / inability to walk

Dysarthria

NO limb weakness initially (unless brainstem compression)

Red Flags

⚠ NEUROSURGICAL EMERGENCY — rapid deterioration from brainstem compression

⚠ Surgical evacuation if ≥3cm diameter OR GCS declining OR hydrocephalus

⚠ Decerebrate posturing = brainstem compression → immediate surgery

Prognosis

Bimodal: excellent if early surgery; devastating without

Most 'surgically treatable' ICH. With early decompression, can achieve excellent recovery (mRS 0–2). Without surgery, brainstem compression is often fatal.

Expected mRS: 0–2 (post-surgery) / 5–6 (untreated)

Aneurysmal rupture (~85%)

Clinical Features

Thunderclap headache ('worst headache of my life') — sudden onset, maximal at onset

Meningism (neck stiffness, photophobia)

Loss of consciousness (transient or sustained)

Grading: Hunt-Hess I (mild headache) → V (coma)

Red Flags

⚠ Rebleeding: highest risk first 24h. Aneurysm must be secured within 24h (Class I)

⚠ Delayed cerebral ischaemia (DCI): peak day 4–14. Nimodipine 60mg q4h × 21 days

⚠ Acute hydrocephalus → urgent EVD

⚠ Avoid prophylactic phenytoin (worse cognitive outcomes). Use levetiracetam if needed

Prognosis

30-day mortality ~35%

Hunt-Hess I–II: ~85% good outcome. Grade III: ~50%. Grade IV–V: <20%. Survivors: ~50% have permanent cognitive deficits.

Expected mRS: 0–2 (low grade) / 4–6 (high grade)

Complications & Red Flags

Across all stroke subtypes

🩸

Haemorrhagic Transformation

Timing: 24h–14d (peak 48–72h)

Risk: Large infarct, reperfusion, anticoagulation, AF

ECASS: HI1/HI2 (petechial, asymptomatic) vs PH1/PH2 (parenchymal haematoma — PH2 causes clinical deterioration). Repeat CT if any decline post-thrombolysis.

🧠

Cerebral Oedema & Herniation

Timing: 24–96h (peak 48–72h)

Risk: TACI, large MCA, younger patients

Malignant MCA oedema: ~80% fatal without intervention. Decompressive hemicraniectomy if age <60, declining GCS, >50% MCA territory. NNT 2 for survival.

🫁

Aspiration Pneumonia

Timing: First 7 days (highest risk days 1–3)

Risk: Dysphagia (~37–78%), reduced consciousness, brainstem stroke

Nil by mouth until formal swallow assessment. Pneumonia is leading cause of non-neurological death post-stroke.

🦵

VTE (DVT / PE)

Timing: Days 2–14+

Risk: Immobility, hemiparesis. DVT up to 50% without prophylaxis

Pneumatic compression (Class I). LMWH from day 1–2 for ischaemic. For ICH: pneumatic immediately; pharmacological after 48h if stable.

⚡

Seizures

Timing: Early <7d; Late >7d

Risk: Cortical involvement (lobar ICH >> deep ICH)

Early seizures: 2–6% ischaemic, ~28% lobar ICH. Do not prophylax routinely. In SAH: avoid phenytoin (worse cognition).

😞

Post-Stroke Depression

Timing: Weeks to months (peak 3–6 months)

Risk: Pre-existing depression, severe disability, social isolation

Affects ~19–33%. Impairs rehab engagement. Screen with PHQ-9. SSRIs first-line.

Prognostic Scores

Quick reference

ICH Score

Hemphill et al. Stroke 2001

GCS 3–4

GCS 5–12

GCS 13–15

ICH volume ≥30 cm³

IVH present

Infratentorial origin

Age ≥80 years

30-Day Mortality

13%

26%

72%

97%

100%

NIHSS → Prognosis

Saver & Altman, Stroke 2012

0–5

Minor

~70–80% independent (mRS 0–2)

6–10

Moderate

~45–55% independent

11–15

Moderate–Severe

~20–35% independent

16–20

Severe

~10–20% independent

>20

Very Severe

<5% independent; high mortality

Hunt-Hess Grade (SAH)

AHA/ASA 2023 SAH Guideline

I Asymptomatic or mild headache

~70% good outcome

II Moderate–severe headache, nuchal rigidity

~60% good outcome

III Drowsy, mild focal deficit

~50% good outcome

IV Stupor, moderate–severe hemiparesis

~20% good outcome

V Coma, decerebrate posturing

<10% good outcome