Medicine — Neurology, NMC MBBS licence examination syllabus (Nepal Medical Council).
Stroke: two opposite diseases wearing the same face
You cannot tell which one you are looking at, and giving the wrong treatment kills.
A patient arrives with a dense right hemiparesis and no speech. You know within seconds that this is a stroke. What you cannot know — not from the history, not from the examination, not from any amount of clinical experience — is whether a vessel is blocked or burst.
That matters more here than almost anywhere else in medicine, because the treatments are opposites. An ischaemic stroke wants the blood thinned. A haemorrhagic stroke wants the bleeding stopped. Thrombolyse an intracerebral haemorrhage and you will kill the patient. This is why the CT scanner sits at the centre of stroke care, and why "scan before you treat" is not caution but the entire logic of the pathway.
🩺 Where this lives: The single commonest avoidable error in suspected stroke is not a missed diagnosis — it is a missed hypoglycaemia. A blood glucose of 1.8 produces a convincing hemiparesis with dysphasia, indistinguishable at the bedside from a middle cerebral artery occlusion. It reverses completely within minutes of glucose. A capillary glucose takes seconds, costs nothing, and is the reason it appears in every stroke protocol ahead of the imaging.
The division that governs everything
Hold on to the asymmetry in that figure. Roughly 85% of strokes are ischaemic, so the odds favour it — but the 15% you would harm are the reason you cannot act on odds. A CT costs minutes; getting this wrong costs the patient.
WHY THE CT IS NON-CONTRAST, AND WHY IT IS URGENT
FRESH BLOOD is bright (hyperdense) on CT immediately.
→ so a non-contrast CT reliably EXCLUDES haemorrhage
straight away, which is the decision you need.
EARLY INFARCTION is often INVISIBLE for hours.
→ so a "normal" CT in a patient with an obvious deficit
is the EXPECTED finding in early ischaemic stroke.
It does not mean there is no stroke — it means there
is no bleed, which is precisely what you asked.
This asymmetry catches people out. The scan is not there
to prove ischaemia. It is there to rule out blood.
Localising the lesion
The deficit tells you which artery, because each supplies a defined territory. This is anatomy doing diagnostic work.
💡 Exam angle: the face-and-arm versus leg distinction is asked constantly, and it comes straight from the homunculus. The motor strip runs over the top of the hemisphere with the leg draped down the medial surface — anterior cerebral territory — while the face and hand occupy the lateral convexity, which the middle cerebral artery supplies. So "leg weaker than arm" points anterior; "face and arm weaker than leg" points middle. You can derive it rather than memorise it.
TWO PATTERNS WORTH RECOGNISING INSTANTLY
CROSSED SIGNS — face on one side, body on the other
Cranial nerve nuclei are in the brainstem and supply
the SAME side; the long tracts cross BELOW them. So a
lesion between the two produces ipsilateral facial and
contralateral limb signs.
→ localises to the BRAINSTEM, not the hemisphere.
LACUNAR SYNDROMES — small deep vessel disease
PURE motor, or PURE sensory, with NO cortical signs:
no aphasia, no neglect, no visual field defect.
Strongly associated with hypertension.
The absence of cortical signs is the clue.
Transient ischaemic attack
A TIA is a transient neurological deficit from focal ischaemia without infarction. The old "less than 24 hours" definition has largely given way to a tissue-based one, because most true TIAs resolve within an hour and many "TIAs" lasting hours turn out to have infarcted on MRI.
The clinically important point is not the definition — it is that a TIA is a warning. Stroke risk is highest in the first days afterwards, which makes a resolved TIA an urgent problem rather than a reassuring one. A patient whose symptoms have completely gone still needs same-day assessment, antiplatelet therapy and investigation of the source. "It got better" is the reason these patients get sent home and return with a completed stroke.
The acute pathway
REPERFUSION IN ISCHAEMIC STROKE
THROMBOLYSIS
Time-critical: benefit falls steeply from onset, so the
eligibility window is narrow and measured from the
TIME LAST KNOWN WELL.
Excluded by: haemorrhage on CT, recent surgery or major
trauma, active bleeding, previous intracranial
haemorrhage, uncontrolled severe hypertension, and
(importantly) UNKNOWN onset time — which is why
"woke up with it" strokes are difficult.
THROMBECTOMY
Mechanical clot retrieval for LARGE-VESSEL occlusion.
A longer window than thrombolysis in selected patients,
and it needs vessel imaging to identify the target.
IF NEITHER IS INDICATED
Antiplatelet therapy, started after haemorrhage has
been excluded — and, if thrombolysed, deferred until
repeat imaging at 24 hours.
💡 Exam angle: blood pressure in acute stroke behaves counter-intuitively. In ischaemic stroke, the tissue around the infarct is being perfused through collaterals at the edge of viability, so dropping the pressure aggressively can extend the infarct — hypertension is usually tolerated unless the patient is being thrombolysed or the pressure is extreme. In haemorrhagic stroke the logic reverses: lowering pressure limits haematoma expansion. Same vital sign, opposite management, decided by the CT.
What else does this
Secondary prevention
The acute treatment addresses this stroke. Secondary prevention addresses the next one, and it is where most of the lifetime benefit sits.
🔍 After an ischaemic stroke or TIA
AntiplateletLong-term antiplatelet therapy — unless the stroke was cardioembolic from atrial fibrillation, in which case anticoagulation replaces it. Getting this distinction right is the single highest-yield decision in prevention.
Atrial fibrillationAnticoagulate. AF causes stasis in the left atrium, thrombus forms, embolises to the brain — and antiplatelets are substantially less effective than anticoagulation against that mechanism.
StatinHigh-intensity, for the same atherosclerotic reasons as in coronary disease.
Blood pressureThe single most important modifiable risk factor for stroke — treated after the acute phase, not during it.
Carotid stenosisSymptomatic severe stenosis on the relevant side may warrant intervention; investigate patients with anterior circulation events.
Diabetes, smoking, alcoholThe familiar list — and, as in the diabetes chapter, cardiovascular risk management is one subject wearing several names.
Complications
EARLY
ASPIRATION PNEUMONIA the reason a SWALLOW SCREEN comes
before anything by mouth, including
oral medication and sips of water
CEREBRAL OEDEMA peaks days 2–5; large infarcts can
cause fatal midline shift
HAEMORRHAGIC TRANSFORMATION of an infarct
SEIZURES
DEEP VEIN THROMBOSIS from immobility
LATER
SPASTICITY and CONTRACTURES
PRESSURE SORES
POST-STROKE DEPRESSION — common and under-recognised
COGNITIVE IMPAIRMENT
SHOULDER SUBLUXATION in a flaccid arm
Most of these are PREVENTABLE with good nursing, early
mobilisation and rehabilitation — which is exactly why a
stroke unit outperforms a general ward.
Clinical reasoning: four presentations
🔍 Case 1 — the reversible mimic
PresentationA 71-year-old on gliclazide is found confused with a right facial droop and right arm weakness. The stroke team is called.
Key clueA sulfonylurea — a drug that causes hypoglycaemia.
ReasoningHypoglycaemia reproduces focal deficits convincingly, including hemiparesis and dysphasia. It is instantly reversible, and missing it means treating a metabolic problem as a vascular one.
AnswerCheck the capillary glucose before anything else. If low, treat it and reassess — the deficit typically resolves within minutes. Only if it persists does this become a stroke pathway.
🔍 Case 2 — the normal scan
PresentationA 64-year-old with a dense left hemiparesis of 50 minutes. Non-contrast CT is reported as normal. A colleague concludes there is no stroke.
TrapReading a normal CT as excluding stroke.
ReasoningEarly infarction is frequently invisible on CT for several hours. The scan's purpose was to exclude haemorrhage, and it has done that — which is exactly what makes the patient a thrombolysis candidate.
AnswerA normal CT with an acute focal deficit supports ischaemic stroke. Assess urgently for thrombolysis or thrombectomy. The normal scan is the green light, not the all-clear.
🔍 Case 3 — the resolved deficit
PresentationA 68-year-old had 20 minutes of right arm weakness and slurred speech yesterday, now completely resolved. He feels fine and wants to go home. Pulse is irregularly irregular.
The distractorFull recovery reads as reassurance.
ReasoningThis is a TIA, and stroke risk is highest in the days immediately after. The irregularly irregular pulse suggests atrial fibrillation — a cardioembolic source, and one that changes prevention from antiplatelet to anticoagulation.
AnswerUrgent same-day assessment, ECG to confirm AF, imaging and carotid assessment, and start secondary prevention now. "It got better" is why these patients are sent home and return with a completed stroke.
🔍 Case 4 — the localising signs
PresentationA 59-year-old with sudden vertigo, diplopia and unsteadiness. On examination there is left facial weakness with right arm and leg weakness.
Key clueCrossed signs — face one side, body the other.
ReasoningCranial nerve nuclei sit in the brainstem and supply the ipsilateral face; the corticospinal tract crosses lower down. Only a brainstem lesion can produce that combination. The vertigo and diplopia fit posterior circulation.
AnswerPosterior circulation (brainstem) stroke. These are more easily missed than hemispheric strokes because the presentation looks vestibular — and they carry a high risk of deterioration from oedema in a confined space.
Commonly confused
Confusion
The distinction
Why it matters
Ischaemic vs haemorrhagic
Indistinguishable clinically; only CT separates them
The treatments are opposite; thrombolysis into a bleed is fatal.
Normal CT vs no stroke
Early infarcts are often invisible; the CT excludes blood
A normal CT supports thrombolysis rather than excluding stroke.
ACA vs MCA territory
ACA: leg worse. MCA: face and arm worse, plus cortical signs
Derivable from the homunculus rather than memorised.
Cortical vs lacunar
Lacunar has NO aphasia, neglect or field defect
Points to small-vessel disease and a different risk profile.
Hemispheric vs brainstem
Crossed signs localise to the brainstem
Posterior circulation strokes are missed as vertigo.
TIA vs minor stroke
TIA has no infarction; both are emergencies
Resolved symptoms carry the highest short-term stroke risk.
BP in ischaemic vs haemorrhagic
Usually permissive in ischaemia; lowered in haemorrhage
Aggressive lowering can extend an infarct.
Rapid revision
MUST-KNOW FACTS
1. Stroke = sudden focal neurological deficit of vascular origin.
2. About 85% ischaemic, 15% haemorrhagic — clinically indistinguishable.
3. URGENT non-contrast CT before any treatment. No exceptions.
4. CT excludes BLOOD; early infarction is often invisible for hours.
5. A normal CT with an acute deficit supports ischaemic stroke.
6. CHECK THE GLUCOSE — hypoglycaemia mimics stroke and reverses in minutes.
7. Establish TIME LAST KNOWN WELL, not the time found.
8. MCA: face and arm worse than leg; aphasia (dominant) or neglect.
9. ACA: leg worse than arm; personality change.
10. PCA: homonymous hemianopia.
11. Posterior circulation: ataxia, vertigo, diplopia, dysarthria, dysphagia.
12. CROSSED signs (face one side, body the other) localise to the brainstem.
13. Lacunar syndromes: pure motor or pure sensory, NO cortical signs.
14. Thrombolysis is time-critical; unknown onset time usually excludes it.
15. Thrombectomy for large-vessel occlusion, in a longer window.
16. Antiplatelet after haemorrhage excluded; delay 24h if thrombolysed.
17. Haemorrhagic stroke: reverse anticoagulation, control BP, neurosurgical opinion.
18. BP is usually permitted to run high in ischaemic stroke; lowered in haemorrhage.
19. TIA carries the HIGHEST stroke risk in the following days — assess same day.
20. AF-related stroke → ANTICOAGULATE, not antiplatelet.
21. SWALLOW SCREEN before anything by mouth — aspiration is the early killer.
22. Cerebral oedema peaks days 2–5.
23. Stroke unit care independently improves survival and function.
💡 Exam angle: the reliable threads are (a) glucose before imaging, (b) a normal CT not excluding stroke, (c) localising from the deficit — especially crossed signs, (d) a resolved TIA being urgent rather than reassuring, and (e) anticoagulation rather than antiplatelet when AF is the source. Notice again how many turn on a normal or improving finding being the dangerous one.
Syllabus points
Ischaemic versus haemorrhagic and why CT comes first
What a non-contrast CT does and does not show
Arterial territories and their deficits
Crossed signs and brainstem localisation
Lacunar syndromes
Transient ischaemic attack and why it is urgent
The acute pathway and time last known well
Thrombolysis and thrombectomy
Blood pressure management in each stroke type
Stroke mimics
Secondary prevention and the atrial fibrillation decision
Complications and the role of the stroke unit
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