Stroke and intracranial haemorrhage

Ischaemic stroke: physiology

• Normal cerebral blood flow is about 50 mL/100 g/min. Below about 20, neurons stop working (electrical failure); below about 10, ion pumps fail and cells die within minutes.
• The penumbra is tissue that is not working but still alive; it becomes core with time, which is why reperfusion is urgent.
• Pump failure lets sodium and water into cells: cytotoxic oedema, seen as restricted diffusion (bright DWI, dark ADC) within minutes. Severe hypoglycaemia causes the same pattern through energy failure.
• TIA: a focal deficit with no infarction on imaging, usually lasting minutes; high early stroke risk.
• Lacunar infarcts (under 15 mm, internal capsule, basal ganglia, pons) come from lipohyalinosis of penetrating arteries in hypertension and diabetes: pure motor or sensory strokes.
• Border-zone (watershed) infarcts follow low flow: tight carotid stenosis, cardiac arrest or massive haemorrhage with prolonged hypotension (a trauma patient who lost 2 L and dies days later with multiple infarcts between arterial territories).

Imaging an infarct over time

• CT perfusion: penumbra has low flow and long transit time with preserved blood volume; core has low blood volume.
• Haemorrhagic transformation follows reperfusion of necrotic vessel walls (embolic AF strokes).
• Cortical laminar necrosis after cardiac arrest gives gyriform T1 bright signal that is not blood.

Pathology of infarction

• The brain shows liquefactive necrosis; other solid organs coagulate.
• Sequence: red neurons at 12–24 h; neutrophils at 1–3 days; by days 5–10 the infarct is full of foamy macrophages packed with myelin lipid, derived from microglia and blood monocytes (the cleaners); astrocytes make the glial scar at the edge (the scar-makers); a fluid-filled cyst remains.

Venous infarcts and other causes

• Cerebral venous thrombosis: postpartum, combined pill, dehydration. Superior sagittal sinus gives bilateral parasagittal infarcts; straight sinus gives bilateral thalamic oedema. Often haemorrhagic, because raised venous pressure ruptures capillaries, and not in arterial territories.
• Reversible cerebral vasoconstriction syndrome: usually postpartum or after vasoactive drugs; recurrent thunderclap headaches over days, small convexity subarachnoid bleeds, multifocal segmental narrowing ("string of beads") that resolves within about 3 months. Convexity blood is not typical of an aneurysm.
• Hyperperfusion after carotid endarterectomy: chronically dilated vessels have lost autoregulation.
• Hereditary haemorrhagic telangiectasia (autosomal dominant): fragile telangiectases on lips and tongue, recurrent epistaxis, iron deficiency, normal clotting; pulmonary AVMs cause paradoxical stroke and brain abscess, and cerebral AVMs can bleed.

Intracerebral haemorrhage

• The CT angiographic spot sign predicts haematoma growth. Duret haemorrhages in the pons follow downward herniation.

Blood on CT and MRI

• Acute blood is hyperdense (60–80 HU) because packed red cells and globin protein attenuate X-rays; density depends on haematocrit. It becomes isodense at 1–3 weeks.
• Severe anaemia (Hb about 6 g/dL in CKD) gives a low-haematocrit clot, so an acute subdural can be isodense with brain: look for midline shift and effaced sulci. Hyperacute unclotted or mixed blood (swirl sign) can also look lower in density.

Extra-axial haemorrhage

• Berry aneurysms arise at branch points where the media is deficient, commonest at the anterior communicating artery. Associations: ADPKD, coarctation, Ehlers–Danlos.
• If CT is normal, lumbar puncture at 12 hours looks for xanthochromia (bilirubin takes that long to form).
• Vasospasm peaks at days 4–14.
• Abusive head trauma: an infant with vomiting, poor feeding or seizures, bilateral subdurals of different ages and extensive retinal haemorrhages, with normal clotting: shaking with violent acceleration–deceleration tears bridging veins and retinal vessels. Check clotting and metabolic causes, but do not delay child protection.
• Preterm babies bleed from the germinal matrix.

Spinal haemorrhage

• Spinal epidural haematoma (anticoagulation, procedures): from the epidural venous plexus, compresses the cord.
• Spinal AVMs can cause haematomyelia or subarachnoid bleeding.

The body's response to blood loss

• A loss of about 15% causes few signs; moderate haemorrhage (15–30%) gives tachycardia over 100, narrowed pulse pressure and anxiety with normal systolic pressure; hypotension appears beyond about 30%.

Remember Brain infarcts liquefy, and on CT they can disappear for a fortnight before they reappear.

Exam trap Pinpoint pupils in coma with fever and quadriplegia mean pontine haemorrhage, not opioids.

Exam trap An acute subdural can be isodense in a very anaemic patient; look for midline shift and effaced sulci.

How FCPS asks about this

• Foamy lipid-laden cells in a 10-day-old infarct: macrophages from microglia and monocytes.
• Bleeding vessel in subdural haematoma: bridging veins; extradural is the middle meningeal artery.
• Isodense acute subdural in severe anaemia: low haematocrit of the collected blood.
• Postpartum thunderclap headaches with segmental arterial narrowing that resolves: RCVS.
• Infant with subdurals of different ages and retinal haemorrhages: shaking injury.
• Last parameter to normalise after haemorrhage: red cell mass; plasma volume returns first by fluid shift.
• Pinpoint pupils, coma, hyperpyrexia: pontine haemorrhage.