EEG, SLEEP, EVOKED POTENTIALS

EEG

Richard Caton 1875 – 1. Registration of ECoG and evoked potentials

Registration of electrical brain potentials

It reflects function properties of the brain

Hans Berger 1929 – human EEG, basic rhythm of electrical activity alfa (8-13Hz) and beta (14-30)

After 1945 – EEG as a clinical inspection

EEG activity is mostly rhytmic and of sinusoidal shape

rhythm α 8-13 Hz

rhythm µ, rolandický rytmus 8-10 Hz

rhythm υ 4-7 Hz

rhythm δ 3 and less Hz

Rhythm β 14-30 Hz

Normal EEG – lokalization of graphoelement types

Frontal - β activity

parietal – µ, rolandic rhythmus

Temporal - α,υ activity

Temporo-parieto- occipital - α activity

Sevření pěsti Uvolnění pěsti

Otevření očí Zavření očí

Podle Faber Elektroencefalografie

Epilepsy

Epilepsy seizure petit mal (absence)

Spike and wave activity

The seizure was clinically manifest as a staring spell

SLEEP

Nathaniel Kleitman in early 1950s made remarkable discovery:

Sleep is not a single process, it has two distinct phases:

REM sleep is characterized by Rapid Eye Movements

Non-REM sleep

The age-old explanation until 1940s – sleep is simply a state of reduced activity

Moruzzi in late 1950s studied reticular formation: rostral portion (above the pons) contributes to wakefulness. Neurons in the portion of RF below pons normally inhibit activity of the rostral part

Sleep is an actively induced and highly organized brain state with different phases

Sleep follows a circadian rhythm about 24 hours

Circadian rhythms are endogenous – persist without enviromental cues – pacemaker, internal clock – suprachiasmatic ncl. hypothalamus

Under normal circumstances are modulated by external timing cues – sunlight – retinohypothalamic tract from retina to hypothalamus (independent on vision)

Resetting of the pacemaker

Lesion or damage of the suprachiasmatic ncl. – animal sleep in both light and dark period but the total amount of sleep is the same

suprachiasmatic ncl. regulates the timing of sleep but it si not responsible for sleep itself

Average evoked potentialsEvent-related potentials

Routine procedure of clinical EEG laboratories from 1980s

Valuable tool for testing afferent functions

EEG changes bind to sensory, motor or cognitive events

Electrical activity – electrodes placed on the patient’s scalp

Evoked electrical activity appears against a background of spontaneous electrical activity.

Evoked activity = a signal

Background activity = a noise

Signal lower amplitude than noise, it may go undetected (hidden or masked by the noise)

Solution

- by increasing amplitude of the signal – intensity of stimulation

-by reducing the amount of the noise

Signal averaging

Mixture of electrical activity composed of spontaneously generated voltages and the voltage evoked by stimulation

Segments or epochs of equal duration

Start coincides with the presentation of stimulus

Duration varies from 10 to hundrets milliseconds

Brain’s spontaneous electrical activity is random with respect to the signal – sum of many cycles will tend to cancel out. (to zero)

The polarity of the EP will always be the same at any given point in time relative to the evoking stimulus

Evoked activity will sum linearly

How to reduce the amount of the noise

-Superimposition

Simplified diagram illustrating how coherent averaging enhances a low level signal (coherent = EP time locked to the evoking stimulus)

How to reduce the amount of the noise

Description of waveforms:

peaks (positive deflection)

troughs (negative deflection)

Measures:

1. Latency of peaks and troughs from the time of stimulation

2. Time elapsing between peaks and/or troughs

3. Amplitude of peaks and troughs

Comparison of the patient’s recorded waveforms with normative data

Visual-evoked potentials (VEP)

Anatomical basis of the VEP:

Visual-evoked potentials (VEP)

Electrical activity induced in visual cortex by light stimuli

Anatomical basis of the VEP: Rods and Cones

Bipolar neurons

Retina

Ganglion cells

Optic nerve

Optic chiasm

Optic tract

Lateral geniculate bodyOptic radiation

Occipital lobe, visual cortex

Anterior visual pathways

Retrochiasmal pathways

Visual-evoked potentials (VEP)

Stimulus: checkerboard pattern on a TV monitor

The black and white squers are made to reverse

A pattern-reversal rate – from 1to 10 per second

Electrodes - 3 standard EEG electrodes placed over the occipital area and a reference elektrode in a midfrontal area

Analysis time (one epoch) is 250 ms

Number of trials 250 , 2 tests at least to ensure that the waveforms are replicable

Normal VEP

VEPs to pattern-reversal, full-field stimulation of the right eye

Abnormal VEPs

Absence of a VEP

Prolonged P 100 – latency - demyelination of the anterior visual pathways

Amplitude attenuation - compressive lesions

Prolonged P 100 only on left or right eye stimulation – lesion of the ipsilateral optic nerve

Excessive interocular difference in P 100 latency – lesion of the ipsilateral optic nerve

of multiple sclerosis:

Excessive interocular difference in P100 latency

Prolonged absolute latency

Decreased amplitude

Compression of optic nerve, optic chiasm (tumor of pituitary gland or optic nerve glioma)

Decreased amplitude

Prolonged latency of P100

VEPs as a tool in the diagnosis

Brain-stem auditory-evoked potential BAEP

Short-latency somatosensory-evoked potential SSEP

Short-latency somatosensory-evoked potential SSEP

Left median nerve study