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Brain rhythms and how seizures start and spread

  • Mechanism
  • Exam priority: medium

The EEG records the summed signals of millions of cortical cells firing together; a seizure is that synchrony running out of control.

Updated

Also called: EEG generation, Paroxysmal depolarizing shift, Spike-and-wave

See it in 3D: Thalamus · Hippocampus · Temporal lobe

What it is

Scalp EEG waves come from synaptic currents in the dendrites of cortical pyramidal cells, which become visible only when many cells act in step; the thalamus paces much of this rhythm. A seizure starts when excitation outweighs inhibition in a group of neurons, they fire in bursts together, and the burst escapes local inhibition to spread. Antiseizure drugs work by restoring that balance.

How it works, step by step

  1. Excitatory synapses on the apical dendrites of pyramidal cells create current sinks and sources; the aligned cells act like small batteries the scalp can detect.
  2. Thalamic reticular neurons inhibit relay neurons rhythmically; when relay neurons rebound they drive the cortex in step, pacing alpha and sleep spindles.
  3. In an epileptic focus, too little GABA inhibition or too much glutamate excitation lets a neuron group depolarize together (paroxysmal depolarizing shift).
  4. Each shift is followed by a hyperpolarization; this is what the EEG shows as an interictal spike and wave.
  5. If surrounding inhibition fails, for example as extracellular K⁺ rises and GABA inhibition fades, the burst recruits neighbors and becomes a seizure.
  6. Spread along cortical and thalamocortical links can turn a focal seizure into a bilateral tonic-clonic one.
  7. In absence epilepsy, hyperpolarized thalamic neurons de-inactivate T-type Ca²⁺ channels and fire bursts that lock cortex and thalamus into a 3 Hz loop.
  8. Seizures stop as neurons are inhibited and exhausted; the postictal state reflects this depressed activity.

Action potential

Action potential: Neuron 012345−100−80−60−40−200+20+40Time (ms)Membrane potential (mV)Rest −70 mVThreshold −55 mVARPRRPRestStimulusDepol.Repol.AHP

Rest −70 mVThreshold −55 mVPeak +35 mVDuration ≈ 1–2 ms

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

  • Mainly Na⁺
  • Mainly K⁺
  • Rest
  • Threshold
  • ARP: absolute refractory period
  • RRP: relative refractory period
A single neuron's spike; the EEG instead adds up slower synaptic currents from thousands of aligned cells.

EEG rhythms

RhythmFrequencyTypical setting
Beta> 13 HzAlert, focused; increased by benzodiazepines
Alpha8–13 HzAwake, relaxed, eyes closed; blocked by eye opening
Theta4–7 HzDrowsiness, light sleep; normal in children
Delta< 4 HzDeep (slow-wave) sleep; focal or diffuse disease when awake
3 Hz spike-and-wave≈ 3 HzAbsence seizure

Clinical notes

  • Hyperventilation lowers PCO₂ and can provoke absence seizures; it is used to bring them out during an EEG.
  • Status epilepticus is a seizure lasting 5 minutes or more, or repeated seizures without recovery; prolonged seizures exhaust inhibition and become harder to stop.
  • In Latin America, neurocysticercosis is a leading cause of acquired focal epilepsy: cysts irritate the surrounding cortex.

Test yourself

Think of the answer, then tap the question to see it.

Why does the scalp EEG reflect synaptic potentials rather than action potentials?

Action potentials are brief and poorly aligned; slower dendritic synaptic currents in parallel pyramidal cells add up when synchronous and are large enough to reach the scalp.

A child has brief staring spells with a 3 Hz spike-and-wave EEG. Which channel underlies this rhythm?

T-type (low-threshold) Ca²⁺ channels in thalamic relay neurons, which fire rebound bursts in a thalamocortical loop; ethosuximide blocks them.

What is the paroxysmal depolarizing shift?

A large, prolonged depolarization of a group of neurons with a burst of action potentials, driven by glutamate and Ca²⁺ currents; it is the cell basis of the interictal spike.

How do phenytoin and carbamazepine reduce seizure spread?

They stabilize the inactivated state of voltage-gated Na⁺ channels, which limits high-frequency repetitive firing while sparing normal firing.

Why might hyperventilation provoke an absence seizure?

It lowers PCO₂ and raises pH, which increases neuronal excitability and favors thalamocortical burst firing.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: EEG: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Focal Onset Seizure (StatPearls (NCBI Bookshelf), 2025); Generalized Tonic-Clonic Seizure (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.