NeurologyTier 2Topic

Metabolism of the brain

Energy demand

The brain is ~2% of body weight but consumes ~20% of resting oxygen and ~25% of glucose - almost entirely dependent on continuous aerobic glucose metabolism, with negligible energy stores
Consequence: irreversible neuronal injury within minutes of complete ischaemia/hypoxia
This near-zero reserve underlies the urgency of cardiac arrest resuscitation, stroke thrombolysis, and status epilepticus management - "time is brain" in a literal metabolic sense

Glucose is the obligate substrate under normal conditions; during prolonged starvation/ketosis, ketone bodies can substitute for a substantial proportion of cerebral energy needs (the basis of the ketogenic diet in refractory epilepsy)
Excitotoxicity: ischaemia/hypoglycaemia -> ATP depletion -> failure of Na+/K+-ATPase -> neuronal depolarisation -> excess glutamate release -> NMDA receptor overactivation -> Ca2+ influx -> cell death - the final common pathway of most acute neuronal injury (stroke, status epilepticus, traumatic brain injury)
Astrocyte-neuron lactate shuttle - astrocytes take up glucose and produce lactate, exported to neurons as an auxiliary fuel, particularly during high activity

Hypoglycaemia is treated as an emergency reversible cause of any acute neurological presentation - always check glucose first in altered consciousness/stroke-mimic presentations
Basis for targeted temperature management post-cardiac arrest - reduces cerebral metabolic rate and excitotoxic injury
Basis for the ketogenic diet in drug-resistant epilepsy - alters neuronal excitability partly via ketone body metabolism

Hypoglycaemic brain injury, hypoxic-ischaemic encephalopathy, status epilepticus, ketogenic diet therapy

Selective vulnerability - certain neuron populations (hippocampal CA1, cerebellar Purkinje cells, watershed cortex) are disproportionately sensitive to hypoxic-ischaemic injury, explaining characteristic patterns of injury after cardiac arrest

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