The Normal EEG

Question 1

Cortical layers

Answer 1

Six horizontal layers - layer I most superficial underneath the pial surface vs layer VI deepest overlying subcortical white matter:
Layer I Molecular layer containing dendrites and axons from other layers
Layer II External granular layer containing cortico-cortical connections
Layer III External pyramidal layer containing cortico-cortical connections
Layer IV Internal granular layer receiving input from thalamus
Layer V Internal pyramidal layer sending output to subcortical structures
Layer VI Multiform layer sending output to thalamus

Question 2

Cortico-cortical connections are in which layers?

Answer 2

Extensive horizontal cortico-cortical connections in layers I, II, and III make up the vast majority of the cortical synapses.

Question 3

Thalamo-cortical connections are in which layers? What type of regulation and thalamic nucleus is involved?

Answer 3

Layers IV (input from thalamus) and VI (output to thalamus)

Thalamocortical projections have an important role in modulating inhibition via thalamic fibers from the reticular nucleus of the thalamus.

Question 4

Where does the electrical activity from the EEG arise from?

Answer 4

The extracellular field potential generated by changes in membrane potential of neurons for the most part with some contribution from glial cells.

Question 5

What is the equilibrium potential for an ion?

Answer 5

The membrane potential at which there is no net movement of that ion across the cell membrane.

Question 6

The resting membrane potential of a neuron…

Answer 6

…Is the membrane potential at which there is no net flow of ions across the cell membrane and typically −70mV, the inside of the neuron being negative in relation to the outside.

The resting membrane potential is determined by the movement of potassium, sodium, and chloride ions along their electrochemical gradient across the cell membrane.

The major contributor of resting membrane potential is the potassium leak channels with a net outward flow of potassium ions (K+) under resting conditions.

Question 7

An action potential is generated…

Answer 7

…when the negativity in the interior of the neuron, i.e., the resting membrane potential, decreases to a critical point (typically around −40mV). The voltage-gated sodium channels play a major role in the generation and propagation of action potential by allowing sodium to enter into the soma. Once generated, the action potential—a short duration (usually less than 2ms) high-amplitude wave of depolarization—travels through the neuronal processes and reaches synapse, a specialized contact between neurons usually between axons and dendrites.

Question 8

Neurotransmitters are released from the presynaptic terminal when…

Answer 8

…an action potential causes sufficient change in the voltage (depolarization) at the presynaptic terminal to activate voltage-gated calcium channels allowing calcium to enter into the presynaptic terminal.

This triggers a cascade of events leading to the fusion of presynaptic vesicles with the membrane of the presynaptic terminal, thereby releasing neurotransmitter molecules into the synaptic cleft.

Binding of neurotransmitters to the receptors on the postsynaptic terminal activates ion channels associated with them, allowing the passage of ions leading to local changes in membrane potential

Question 9

Postsynaptic potential

Answer 9

Local changes in membrane potential following activation of ion channel secondary to biding of neurotransmitters on the postsynaptic terminal

Non-propagated small-amplitude potentials lasting 10–100ms.

Can be excitatory (excitatory postsynaptic potential (EPSP)) or inhibitory (inhibitory postsynaptic potential (IPSP)) depending on the type of ion channel activated and the electrochemical gradient for ions that can pass through the channel.

Question 10

EPSP

Answer 10

EPSPs generally result from an inward flow of positive ions such as sodium or calcium and cause depolarization (excitation), thus decreasing the threshold for triggering an action potential in the postsynaptic terminal.

Question 11

IPSP

Answer 11

On the other hand, IPSPs result from an inward flow of negative ions (e.g., chloride) or outward flow of positive ions (e.g., potassium) and cause hyperpolarization (inhibition), thus increasing the threshold for triggering an action potential in the postsynaptic terminal.

Question 12

A single EPSP or IPSP…

Answer 12

…is not sufficient enough to move the membrane potential of the postsynaptic terminal to or away from the threshold for triggering of action potential.

Summation of several PSPs is necessary for that purpose.

Question 13

Summation of PSPs

Answer 13

Such summation can be spatial (summation of several PSPs in the vicinity) or temporal (summation of several PSPs occurring in quick succession).

Question 14

Extracellular field potentials from PSPs and the EEG

Answer 14

A large number of EPSPs and IPSPs generated in a complex network of neurons alter the overall excitability of the neurons in the network. Such PSPs generate an extracellular field potential that changes over time which is believed to be the basis of potentials recorded on EEG.

The extracellular field potential is a secondary phenomenon resulting from the development of potential gradients between areas of localized membrane potential change and the remaining areas of the neuronal membrane.

Question 15

EPSP and a “sink’
IPSP and a “source’

Answer 15

Referring to flow of positive ions

A ‘sink’ is generated at the site of an EPSP because of an inflow of positive ions into the localized area of the neuron, and there is a corresponding ‘source’ at a distance where positive ions come out of the neuron; current flows from the ‘source’ to the ‘sink’ in the extracellular space giving rise to the extracellular field potential.

Question 16

EPSP and IPSP recording negative and positive potentials respectively

Answer 16

Thus, a recording electrode close to the synapse receiving an excitatory input (EPSP) would record a negative potential because of an inward flow of positive ions causing negativity in the extracellular space nearby, whereas a deep recording electrode at a distance would record positivity because of an outflow of positive ions associated with the current flowing through the extracellular space.

The reverse is true for an inhibitory input (IPSP): A recording electrode close to the synapse receiving an inhibitory input (IPSP) would record a positive potential because of an inward flow of negative ions (or an outward flow of positive ions), whereas a recording electrode at a distance would record negativity because of an outflow of negative ions (or an inflow of positive ions) associated with the current flowing through the extracellular space.

Therefore, polarity of extracellular field potentials recorded by surface electrodes on EEG depends on the direction of current flow as well as on the position of the electrode relative to the location of the generator.

This translates to the fact that superficial EPSPs and deep IPSPs will show the same polarity (negative) on a surface recording electrode. Likewise, superficial IPSPs and deep EPSPs will show the same polarity (positive) on a surface recording electrode

Question 17

Pyramidal neurons in the cerebral cortex and vertical dipoles

Answer 17

Pyramidal neurons in the cerebral cortex are arranged in vertical columns with their cell bodies typically in the layer III (external pyramidal) or V (internal pyramidal) and their processes (dendrites and axons) spanning the entire column and receiving thousands of synaptic contacts. This allows for summated potentials with a vertical dipole or a dipole oriented at an angle to the recording electrodes, which can be recorded on the EEG.

Question 18

Horizontal dipoles

Answer 18

On the other hand, summated potentials resulting in horizontal dipoles (oriented parallel to the recording electrodes) cannot be generally recorded on EEG.

Question 19

To produce a scalp EEG signal, ______ is required.

Answer 19

To produce a scalp EEG signal, 6cm2 or more of synchronously active area of cortex is required.

Question 20

Distance and scalp EEG

Answer 20

Scalp electrodes record volume-conducted potentials. Signal decreases proportionally to the square of the distance between the source and the electrode.

Question 21

Electrode view and the solid angle

Answer 21

The potential recorded at the electrode is proportional to the solid angle subtended by the dipole layer.

Question 22

Vertical vs horizontal dipoles

Answer 22

As the orientation of the dipole becomes progressively less radial and more tangential to a recording electrode, the electrode records a voltage field of lesser amplitude. If the dipole is directly below the electrode but it is perfectly tangential, the electrode records no potential because of its location on the zero isopotential line of the source scalp field.

Question 23

Recording of fluctuating field potentials

Answer 23

Can be recorded via conventional EEG

When an afferent fiber forming an excitatory synapse on an apical dendrite near the surface produces bursts of action potentials interrupted by periods of quiescence, EPSPs sum up during the bursts giving rise to fluctuating field potentials.

When recording from surface is done with an amplifier with a finite time constant (as in conventional EEG), such fluctuations in field potential are recorded as waveforms.

Question 24

Recording of depolarization shift

Answer 24

Sustained firing of the afferent fiber leads to sustained depolarization of the apical dendrites causing a depolarization shift which is not reflected on the surface in conventional EEG recorded with an amplifier with a finite time constant. Sustained changes in field potential (baseline shifts) can be recorded using a direct current or DC amplifier that has an infinite time constant.

Question 25

Field potentials during epileptic activity

Answer 25

Field potentials generated during epileptic activity are of higher amplitude than those generated by nonepileptic activity because epileptic field potentials are the result of highly synchronized neuronal activity.

Question 26

Focal epileptic activity and PDS

Answer 26

During focal epileptic activity, negative potentials of high amplitude, which repeat themselves in stereotyped form and periodicity, can be recorded from the area. Such oscillations of field potential occur in parallel with the fluctuation of membrane potential which is the characteristic of the epileptiform activity of individual neurons (Fig.1.8).

This is known as paroxysmal depolarization shift (PDS) which starts with a steep depolarization that triggers a series of action potentials followed by a plateau of continued depolarization; this is followed, after 80–100ms, by a steep repolarization with or without an after-going hyperpolarization.

Question 27

Paroxysmal depolarization shift

Answer 27

This is known as paroxysmal depolarization shift (PDS) which starts with a steep depolarization that triggers a series of action potentials followed by a plateau of continued depolarization; this is followed, after 80–100ms, by a steep repolarization with or without an after-going hyperpolarization.

Question 28

Field potentials on surface vs deep cortical layers

Answer 28

It is important to note that field potentials recorded from the surface may differ from those recorded from different layers of the cortex. This has been shown in animal experiments using local application of penicillin as trigger for focal epileptiform activity. Intracortical potential distribution that determines the occurrence of associated descending activity to the spinal cord (that can reflect motor activity) may be different for the same epileptiform activity recorded from the surface; negative field potential in the layer V only was associated with the corresponding spinal field potentials.

Question 29

GTC

Answer 29

When tonic–clonic activity is triggered in experimental animals by repeated injections of pentylenetetrazol, and membrane potential of a pyramidal tract in the layer V of the cortex is recorded during a convulsive seizure, typical PDSs can be seen, which correlate with the potential fluctuations noted in the DC recording—with superficial negative potential fluctuations (corresponding to synchronized depolarization [positive ions moving inward to move the membrane potential form -70 closer to 0] of pyramidal neurons) in the beginning and with superficial positive potential fluctuations (corresponding to postictal hyperpolarization of pyramidal neurons) at the end of the convulsive seizure (Fig.1.9).

Question 30

Spreading depression

Answer 30

A strong and rapid depolarization of neurons that slowly propagates (3–5mm/min) in nervous tissue

It has a prominent high-amplitude negative component followed by a smaller amplitude but longer duration positive wave; an initial small positive component may sometimes be seen.

SD can have maximal amplitude of 5–30mV and can last for 30–90s.

An initial brief period of excitation followed by prolonged depression, which is then replaced by sustained increase in the neuronal activity is the key feature of SD. The initial and late increase in excitability seen in SD correlates with the burst of action potentials and intense synaptic noise associated with synchronized neuronal activity.

SD has been implicated in the pathophysiology of several disorders including migraine, epilepsy, transient global amnesia, cerebrovascular disease, head injury, and spinal cord disorders.

Question 31

Areas of brain involved in brain rhythms - generation, synchronization, and desynchronization

Answer 31

The cerebral cortex, thalamus, and several generalized modulatory systems arising from the brain stem core, posterior hypothalamus, and basal forebrain are thought to be responsible for the generation, synchronization, and desynchronization of brain rhythms (regularly recurring waveforms of similar shape and duration) that can be recorded on EEG.

Question 32

Slow delta rhythms

Answer 32

Delta activity represents 0–4Hz fr
equency range. Thalamus and cortex are the two sources of delta activity. Thalamocortical neurons display rhythmic bursts of high-frequency spikes with an interburst frequency of 1–2Hz which results from interplay between a transient calcium current (I t) and hyperpolarization-activated cation current (I h). Delta activity has been noted in cats with thalamic lesion suggesting a cortical source for delta oscillations as well.

Question 33

The slow oscillation and the K-complex

Answer 33

The K-complex is a result of a sequence of depolarizing–hyperpolarizing episodes within a slow cortical oscillatory cycle. Such slow cortical oscillations are seen during sleep. Slow oscillation becomes more regular and faster with deepening of sleep. Firing rate of the midbrain reticular formation and mesopontine cholinergic neurons decrease at sleep onset removing steady excitatory drive to thalamocortical neurons. This leads to progressive hyperpolarization of these neurons which corresponds to deepening of sleep.

Question 34

Theta rhythms

Answer 34

Theta rhythms are in the 4–7Hz frequency range, which is conspicuous in limbic regions in various animal species and in humans. It is thought to represent a dynamic state arising from neuronal networks in the hippocampus associated with spatial navigation and memory processes.

Question 35

Faster rhythms: Beta and gamma rhythms

Answer 35

Beta and gamma rhythms are faster rhythms associated with wakeful state or REM sleep. They arise when spindle and slower EEG rhythms are suppressed (probably mediated by acetylcholine, serotonin, and norepinephrine) upon stimulation of brain stem structures. Episodes of cortical oscillations faster (100–600Hz) than beta–gamma frequency called ripples ripples (100 to 200Hz), or fast ripples (>200Hz) have been described under both normal conditions and epileptic seizures. Ripples probably reflect synchronized IPSPs, whereas fast ripples appear to represent bursts of population spikes. While high-frequency oscillations like ripples and fast ripples may be normal, recent studies indicate that they may be the marker of epileptogenic region.

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Question 35

Alpha rhythms

Answer 35

Alpha rhythm represents the frequency range of 8–13Hz. Aside from occipital cortex, alpha rhythm can be recorded from the somatosensory cortex (also called mu rhythm) and temporal cortex (also called tau rhythm). Alpha rhythms are mainly generated from the cortex with only moderate dependence on the thalamus.

Question 36

Spindle (sigma) rhythms:

Answer 36

Spindles (7–14Hz) originate from the thalamus and are considered to be the first signs of EEG synchronization during early stages of sleep. The reticular nucleus of the thalamus is regarded as the pacemaker of the spindles.