Eeg Sleep Iom Ver

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EEG nd Sleep

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Eeg Sleep Iom Ver

  1. 1. EEG, SLEEP, EVOKED POTENTIALS
  2. 2. 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
  3. 3. EEG activity is mostly rhytmic and of sinusoidal shape rhythm  8-13 Hz rhythm  , rolandický rytmus 8-10 Hz rhythm  4-7 Hz rhythm  3 and less Hz Rhythm  14-30 Hz
  4. 4. Normal EEG – lokalization of graphoelement types Frontal -  activity parietal –  , rolandic rhythmus Temporal -  ,  activity Temporo-parieto- occipital -  activity Sevření pěsti Uvolnění pěsti Otevření očí Zavření očí Podle Faber Elektroencefalografie
  5. 10. Epilepsy
  6. 11. Epilepsy seizure petit mal (absence) Spike and wave activity The seizure was clinically manifest as a staring spell
  7. 12. 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
  8. 13. 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
  9. 17. Average evoked potentials Event-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
  10. 18. <ul><li>Electrical activity – electrodes placed on the patient ’ s scalp </li></ul><ul><li>Evoked electrical activity appears against a background of spontaneous electrical activity. </li></ul><ul><li>Evoked activity = a signal </li></ul><ul><li>Background activity = a noise </li></ul><ul><li>Signal lower amplitude than noise, it may go undetected (hidden or masked by the noise) </li></ul><ul><li>Solution </li></ul><ul><li>- by increasing amplitude of the signal – intensity of stimulation </li></ul><ul><li>by reducing the amount of the noise </li></ul>
  11. 19. 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 activit y 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
  12. 20. <ul><li>How to reduce the amount of the noise </li></ul><ul><li>Superimposition </li></ul>
  13. 21. 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
  14. 22. 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
  15. 23. Visual-evoked potentials (VEP) Anatomical basis of the VEP:
  16. 24. 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 body Optic radiation Occipital lobe, visual cortex Anterior visual pathways Retrochiasmal pathways
  17. 25. 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
  18. 26. Normal VEP VEPs to pattern-reversal, full-field stimulation of the right eye
  19. 27. 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
  20. 28. 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
  21. 29. Brain-stem auditory-evoked potential BAEP Short-latency somatosensory-evoked potential SSEP
  22. 30. Short-latency somatosensory-evoked potential SSEP Left median nerve study

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