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EEG nd Sleep
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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