Two per cent of body weight.
Fifteen per cent of the cardiac output.

The minimum high-yield framework

1. The brain is 2% of body weight and receives 12-15% of cardiac output, consuming 20% of total body oxygen.
2. CBF about 50 mL/100 g/min; CMRO₂ about 3.5 mL O₂/100 g/min. Grey matter has about four times the flow and four times the metabolic rate of white.
3. 60% of that energy is electrophysiological and 40% is housekeeping. Anaesthetics abolish only the first; hypothermia reduces both.
4. Glucose, aerobically, and almost nothing else. No meaningful glycogen store, negligible anaerobic capacity, and the barrier restricts what else can be used. Ketones can substitute only after days of starvation.
5. Flow is coupled to metabolism — neurovascular coupling. Raise local activity and local flow rises with it.
6. Reserve is measured in seconds. Consciousness is lost about 10 seconds after circulatory arrest; irreversible injury begins within minutes at normothermia.
7. The cascade below 10 mL/100 g/min is: ATP fails → the Na⁺/K⁺-ATPase fails → depolarisation → calcium entry → glutamate excitotoxicity → enzymatic damage → swelling and death, by necrosis or delayed apoptosis.

About 60% of cerebral energy consumption supports electrophysiological function: generating and propagating action potentials, restoring the ionic gradients afterwards, and synthesising, transporting, releasing and recovering neurotransmitters. The remaining 40% supports cellular homeostasis — the “housekeeping” component: protein turnover, membrane maintenance, organelle function.

1. An obligatory glucose requirement. Under normal conditions glucose is effectively the only fuel. It crosses the blood-brain barrier on the GLUT1 transporter by facilitated diffusion, is not insulin-dependent, and is then metabolised by oxidative phosphorylation. Hypoglycaemia therefore produces neuroglycopenic symptoms and, if severe and prolonged, the same cellular cascade as ischaemia.
2. Obligatory aerobic metabolism. Anaerobic glycolysis yields 2 ATP per glucose against about 30 for complete oxidation — nowhere near enough to run the sodium-potassium ATPase of a whole brain. The brain therefore has no useful anaerobic capacity, and lactate production is a marker of failure rather than an alternative supply.
3. Almost no substrate reserve. Cerebral glycogen is negligible. Consciousness is lost about ten seconds after circulatory arrest, and the reserve of oxygen and glucose in the tissue is exhausted within a few minutes.
4. A restricted menu, set by the barrier. Free fatty acids are largely excluded, so the brain cannot switch to fat the way muscle does. Ketone bodies are the one substantial exception: after several days of starvation, monocarboxylate transporters are upregulated and ketones can supply a large proportion of cerebral energy. This is an adaptation over days, not an acute rescue.

where CMRO₂ is the cerebral metabolic rate for oxygen (mL O₂ per 100 g per minute), CBF is cerebral blood flow (mL per 100 g per minute), CaO₂ is arterial oxygen content and CjvO₂ is jugular venous oxygen content (both mL O₂ per 100 mL of blood).

Read it as a statement about coupling. If metabolic rate is fixed, then a fall in flow must be met by a rise in extraction, and the jugular venous saturation falls. That is exactly what jugular bulb oximetry measures: a falling SjvO₂ means flow has become inadequate for demand, and a rising SjvO₂ means either luxury perfusion or a brain that has stopped extracting. Both are informative and they mean opposite things.

Two accounts of the mechanism coexist, and naming both is worth stating. The traditional feedback account is that increased neuronal activity produces metabolic by-products which act locally as vasodilators. The feed-forward account, better supported by recent data, is that neuronal activity increases flow directly through signalling rather than through a metabolic deficit — the supply arrives before the shortfall does.

The astrocyte is central to all of this. Its processes contact both the synapse and the capillary, so it is anatomically placed to sense activity and to signal to the vessel — which is why it appears again here having already appeared in lesson 1.

Previously examinedOctober 2025 — the special features of cerebral metabolism, the cellular changes below 10 mL/100 g/min, and the physiological basis of cerebral protection. Worked answers in the library

The flow thresholds in the figure explain why an insult can be reversible. Between about 6 and 15 mL/100 g/min the tissue is electrically silent but structurally alive — the ischaemic penumbra. Restoring flow restores function. Below about 6, membrane failure follows within minutes. The zone between them is the target of every acute intervention in stroke and in traumatic brain injury.

Injury also has two time courses. Necrosis dominates where ischaemia is severe, and is complete within hours. Delayed neuronal death by apoptosis continues for days after the insult, and is the reason a neuroprotective intervention must be assessed at long follow-up — an apparent benefit at 24 hours often disappears by a month.

Why hyperglycaemia and hypoglycaemia are both dangerous after a brain insult

The brain needs glucose and cannot store it, so hypoglycaemia is directly injurious. But in ischaemic tissue, a high glucose is also harmful: more substrate for anaerobic glycolysis means more lactate and a lower intracellular pH in a cell that is already failing. Normoglycaemia, not a high-normal glucose, is the target.

Why a seizure in a paralysed patient is a metabolic emergency

Seizure activity can raise cerebral metabolic rate by as much as 400%. Flow rises too, but if perfusion is already compromised — by raised intracranial pressure, by hypotension, or by a stenosed vessel — demand outstrips supply and the tissue infarcts. A neuromuscular blocker abolishes the visible seizure without touching the metabolic one, which is the argument for electroencephalographic monitoring in the paralysed patient at risk.

Why temperature is a neuroprotective variable and not a comfort measure

Cerebral metabolic rate changes 6 to 7% per degree Celsius. A patient allowed to run at 38.5 °C after a brain insult has a cerebral metabolic rate roughly 10% above baseline at the moment supply is least able to meet it. Preventing fever is one of the few interventions with a clean physiological rationale and a plausible clinical benefit; it belongs in the plan for every patient with a brain injury.