16.1 Stroke Classification, Brainstem Syndromes & Hyperacute Reperfusion
Key Takeaways
- A total anterior circulation stroke requires all three of higher cortical dysfunction, homonymous hemianopia and motor/sensory deficit affecting at least two of face, arm and leg.
- Lateral medullary (Wallenberg) syndrome from posterior inferior cerebellar artery occlusion causes ipsilateral facial sensory loss, Horner syndrome and ataxia with contralateral body sensory loss.
- Alteplase is given within 4.5 hours of onset after haemorrhage is excluded; mechanical thrombectomy is offered for proximal anterior circulation occlusion, with selected patients treated well beyond 6 hours on perfusion imaging.
Cerebrovascular disease represents one of the most heavily tested topics in MRCP(UK) Part 1. Candidates must master clinical anatomical localization via the Oxford Community Stroke Project (Bamford) classification, hyperacute reperfusion protocols (intravenous thrombolysis and mechanical thrombectomy), physiological blood pressure targets, secondary prevention algorithms, urgent transient ischaemic attack (TIA) pathways, and the emergency management of intracranial haemorrhage.
1. Oxford Community Stroke Project (Bamford) Classification
The Bamford (OCSP) classification is a validated clinical bedside tool used to classify acute ischaemic stroke based entirely on presenting signs and symptoms prior to neuroimaging. It predicts underlying vascular anatomy, infarct volume, risk of early recurrence, and 1-year mortality.
| Classification | Clinical Criteria & Defining Features | Vascular Territory & Anatomy | 1-Year Mortality & Recurrence Risk |
|---|---|---|---|
| Total Anterior Circulation Stroke (TACS) | Complete triad of: <br>1. Hemiparesis and/or hemisensory loss (contralateral face, arm, and leg)<br>2. Homonymous hemianopia (contralateral)<br>3. Higher cortical dysfunction (dysphasia/aphasia, or visuospatial neglect/inattention) | Proximal Middle Cerebral Artery (MCA stem) or Internal Carotid Artery (ICA) terminus occlusion; extensive frontotemporoparietal hemispheric infarction | Highest mortality (~60% at 1 year); low recurrence rate (~6%) because of high early case fatality; high risk of malignant cerebral oedema |
| Partial Anterior Circulation Stroke (PACS) | 2 of the 3 TACS triad components, OR isolated higher cortical dysfunction alone (e.g. pure expressive dysphasia), OR restricted motor/sensory deficit (e.g. monoparesis of one limb or face + arm only) | Branch/distal MCA occlusion (anterior or posterior division), or Anterior Cerebral Artery (ACA) cortical branches | Intermediate mortality (~15% at 1 year); highest early recurrence risk (~17% at 1 year) due to unstable emboligenic arterial or cardiac sources |
| Lacunar Stroke (LACS) | Subcortical stroke presenting with one of four classical lacunar syndromes:<br>1. Pure motor hemiparesis<br>2. Pure sensory stroke<br>3. Sensorimotor stroke<br>4. Ataxic hemiparesis (or clumsy-hand dysarthria)<br>Crucially: NO visual field defect, NO higher cortical dysfunction, NO brainstem signs | Lipohyalinosis and microatheroma of small, deep penetrating end-arteries: lenticulostriate (off MCA), thalamoperforating (off PCA), or paramedian pontine branches. Involves posterior limb of internal capsule, thalamus, or base of pons | Lowest early mortality (~10% at 1 year); intermediate recurrence risk (~10%); best functional recovery if rehabilitation is instituted early |
| Posterior Circulation Stroke (POCS) | Any of the following focal signs:<br>1. Cerebellar dysfunction (ataxia, nystagmus, dysdiadochokinesia)<br>2. Brainstem syndromes / crossed cranial nerve palsies with contralateral long tract motor/sensory deficits<br>3. Isolated homonymous hemianopia or cortical blindness<br>4. Bilateral motor or sensory deficits<br>5. Conjugate gaze palsy or disordered ocular motility | Vertebrobasilar arterial system: Vertebral arteries, Basilar artery, Posterior Cerebral Arteries (PCA), or cerebellar arteries (PICA, AICA, SCA) | Variable mortality (~20–30% at 1 year); high risk of basilar artery thrombosis (which carries >80% mortality if recanalisation is delayed) |
MRCP Exam Pearl: Defining Higher Cortical Dysfunction: In Bamford criteria, higher cortical dysfunction strictly denotes dysphasia/aphasia, visuospatial neglect, apraxia, agnosia, or conjugate gaze deviation away from the hemiparetic side. Dysarthria alone is a motor articulatory symptom and does not count as higher cortical dysfunction; isolated dysarthria with hemiparesis constitutes a lacunar syndrome (LACS).
2. Vascular Brainstem Syndromes
Crossed neurological findings—ipsilateral cranial nerve palsy combined with contralateral body motor or sensory hemiparesis—are the hallmark of brainstem stroke. MRCP Part 1 frequently assesses lateral medullary and paramedian midbrain syndromes:
| Feature / Finding | Wallenberg Syndrome (Lateral Medullary Syndrome) | Weber Syndrome (Paramedian Midbrain Syndrome) |
|---|---|---|
| Culprit Arterial Vessel | Posterior Inferior Cerebellar Artery (PICA) (in ~20%) or culprit parent Vertebral Artery occlusion (in ~80%) | Paramedian perforating branches of the Posterior Cerebral Artery (PCA) or top of the basilar artery |
| Anatomical Structures Involved | 1. Nucleus ambiguus (CN IX, X)<br>2. Spinal trigeminal nucleus & tract (CN V)<br>3. Descending sympathetic tract<br>4. Inferior cerebellar peduncle<br>5. Spinothalamic tract | 1. Oculomotor nerve (CN III) fascicles<br>2. Crus cerebri (cerebral peduncle / descending corticospinal & corticobulbar tracts) |
| Ipsilateral Clinical Signs | - Dysphagia, hoarseness, impaired gag reflex, palatal paralysis (nucleus ambiguus)<br>- Facial pain and temperature sensation loss (spinal trigeminal nucleus)<br>- Horner's syndrome (miosis, partial ptosis, anhidrosis from descending sympathetics)<br>- Cerebellar ataxia, dysmetria, past-pointing (inferior cerebellar peduncle) | - Complete CN III palsy: Ptosis, widely dilated and unreactive pupil, eye positioned "down and out" due to unopposed action of lateral rectus (CN VI) and superior oblique (CN IV) |
| Contralateral Clinical Signs | - Loss of pain and temperature sensation over trunk and limbs (lateral spinothalamic tract) | - Contralateral spastic hemiparesis/hemiplegia of the face, arm, and leg (interruption of corticospinal and corticobulbar fibres in crus cerebri) |
| Sparing / Negative Features | - Corticospinal tract is spared (runs in the medial medulla / anterior pyramid); therefore, there is NO limb motor hemiplegia in Wallenberg syndrome | - Sensation and cerebellar coordination are typically preserved |
3. Acute Ischaemic Stroke: Hyperacute Reperfusion Pathways
Immediate Emergency Neuroimaging
Every patient with suspected acute stroke requires an immediate unenhanced non-contrast CT head to differentiate ischaemic stroke from intracerebral haemorrhage. CT excludes haemorrhage and identifies early ischaemic changes (loss of grey-white matter differentiation, insular ribbon sign, sulcal effacement, hyperdense MCA sign).
Intravenous Thrombolysis (IV Alteplase)
- Indication & Window: Recombinant tissue plasminogen activator (rt-PA, alteplase 0.9 mg/kg, maximum 90 mg; administered as a 10% IV bolus over 1 minute followed by 90% infused over 60 minutes). Recommended for patients presenting within 4.5 hours of known symptom onset (or time last known well) where intracerebral haemorrhage is excluded.
- Absolute Contraindications to Thrombolysis (High-Yield MRCP List):
- Intracranial haemorrhage on current CT, or any past medical history of intracerebral haemorrhage.
- Known intracranial arteriovenous malformation (AVM), aneurysm, or intracranial neoplasm.
- Active internal bleeding, gastrointestinal haemorrhage within previous 21 days, or severe trauma/major surgery within previous 14 days.
- Ischaemic stroke or severe head injury within previous 3 months.
- Coagulopathy: Platelet count $< 100 \times 10^9/\text{L}$, INR $> 1.7$, prothrombin time $> 15\text{ seconds}$, or activated partial thromboplastin time (aPTT) elevated.
- Direct Oral Anticoagulant (DOAC) ingestion within previous 48 hours (unless specific reversal agent administered or sensitive drug level assays prove negligible anticoagulant activity).
- Persistent severe hypertension: Systolic BP $> 185\text{ mmHg}$ or Diastolic BP $> 110\text{ mmHg}$ refractory to rapid intravenous antihypertensive therapy.
- Lumbar puncture or arterial puncture at a non-compressible site within previous 7 days.
Mechanical Thrombectomy (Endovascular Clot Retrieval)
- Standard Indication (0–6 Hours): Recommended within 6 hours of symptom onset for confirmed anterior circulation Large Vessel Occlusion (LVO: intracranial internal carotid artery or proximal middle cerebral artery M1 segment) in patients with independent baseline functional status (modified Rankin Scale mRS 0–2).
- Extended Window (6–24 Hours): Indicated up to 24 hours from last known well (including wake-up strokes) in selected patients demonstrating clinical-core or perfusion mismatch on advanced CT perfusion or diffusion-weighted MRI (DAWN and DEFUSE 3 trial criteria: small ischaemic core with substantial salvageable penumbra).
Blood Pressure Management in Acute Ischaemic Stroke
- Permissive Hypertension Principle: Cerebral autoregulation is disrupted in acute ischaemia; perfusion to the ischaemic penumbra depends passively on mean arterial pressure. Precipitous blood pressure reduction induces penumbral infarction and worsens clinical outcome.
- Guideline-Directed Thresholds (NICE / ESO):
- Non-thrombolysed patients: Do NOT treat blood pressure unless severe hypertension is present: Systolic BP $> 220\text{ mmHg}$ or Diastolic BP $> 120\text{ mmHg}$, or there is concurrent hypertensive target organ damage (e.g. acute aortic dissection, acute pulmonary oedema, hypertensive encephalopathy). If $> 220/120\text{ mmHg}$, lower BP cautiously by no more than $15%$ over the initial 24 hours.
- Thrombolysed / Thrombectomy candidates: Blood pressure must be lowered to $< 185/110\text{ mmHg}$ before initiating alteplase and maintained $< 180/105\text{ mmHg}$ for at least 24 hours post-reperfusion to prevent fatal reperfusion haemorrhagic transformation. First-line IV agents: intravenous labetalol, nicardipine, or hydralazine.
A 58-year-old man presents to the emergency department with sudden onset of vertigo, severe unsteadiness, dysphagia, and hoarseness that began 2 hours ago. On physical examination, he is alert and orientated. Cranial nerve examination reveals right-sided facial sensory loss to pain and temperature, right-sided palatal weakness with diminished gag reflex, right-sided miosis and 2 mm ptosis with intact direct and consensual light reflexes. Limb examination reveals normal motor power (Medical Research Council grade 5/5) throughout all four extremities, but marked dysmetria on right finger-nose testing. Sensory examination demonstrates impaired pinprick and thermal sensation over the left trunk, left arm, and left leg. Which vascular territory is primarily occluded?
A 68-year-old woman is brought to the emergency department by ambulance 90 minutes after developing acute right-sided weakness and an inability to speak. On arrival, her blood pressure is 198/114 mmHg, heart rate is 84 beats/min regular, respiratory rate is 16 breaths/min, and blood glucose is 6.2 mmol/L. Neurological examination confirms a dense right hemiplegia, right homonymous hemianopia, and global aphasia (Total Anterior Circulation Stroke, NIHSS score 19). Non-contrast CT head reveals early loss of insular ribbon definition on the left with no intracranial haemorrhage. What is the most appropriate next step in the emergency management of this patient?