8.11. Electroencephalogram (EEG); sleep phenomena. Learning and memory. Flashcards
I. Electroencephalogram (EEG)
1. What is EEG?
EEG is the recording of neuronal electrical activity that is produced in the cerebral cortex
I. Electroencephalogram (EEG)
2. How are electrodes placed on the skull?
- Electrodes are placed on the skull
- only the generated dipoles originating from pyramidal cells, which are perpendicular to the skull, are detected and will result in EEG waves (μV range)
I. Electroencephalogram (EEG)
3. How are temporal resolution and spatial resolution in EEG?
- Temporal resolution is very good (can detect brain activity within a millisecond timescale)
- The spatial resolution is not so good, making it harder to localize the source precisely in space
=> can increase spatial resolution by increasing the number of electrodes
I. Electroencephalogram (EEG)
4. Describe electrode placement
- 100% is measured between the naison (middle point of nasofrontal suture) and inion (occipital protuberance)
- The electrodes are placed in a way that the distance is divided in a 10% - 4x20% - 10% manner
- Can be used in the mid-sagittal and horizontal section
- 19 electrodes + reference electrodes (typically placed on ear lobes)
I. Electroencephalogram (EEG)
5A. What are the 2 types of recording in EEG?
- Bipolar recording
- Unipolar recording
I. Electroencephalogram (EEG)
5B. Describe bipolar recording
- Both the electrodes are at active site
- Difference of potential between the 2 electrodes is detected
I. Electroencephalogram (EEG)
5C. Describe unipolar recording
- One electrode is active and the other is indifferent (kept at ear lobe)
- By comparing the potential to the reference electrode, we can detect the potential at all other points
I. Electroencephalogram (EEG)
6A. What is montage?
a system in which we can detect the signals between the electrodes
I. Electroencephalogram (EEG)
6B. What are the 4 types of montage?
- Sequential monotage
- Referential montage
- Average reference montage
- Laplacian montage
I. Electroencephalogram (EEG)
6C. What is sequential montage?
difference between two adjacent electrodes
I. Electroencephalogram (EEG)
6D. What is referential montage?
potentials are compared to a reference electrode (e.g. linked
ears)
I. Electroencephalogram (EEG)
6E. What is average reference montage?
reference is the average of all signals
I. Electroencephalogram (EEG)
6F. What is Laplacian montage?
the average of the surround electrodes is subtracted
II. Basic wave types.
1. What are the 5 basic wave types
- Alpha wave
- Beta wave
- Gamma wave
- Theta wave
- Delta wave
II. Basic wave types.
2. What are the characteristics of alpha wave?
- Rhythmic, 8 – 13Hz
- Mostly on occipital lobe
- Amplitude: 20 – 200μV
- Relaxed awake rhythm with eyes closed
- Mental activityalpha waves are replaced by beta waves
- Disappears during sleep
II. Basic wave types.
3. What are the characteristics of beta wave?
- irregular, 14 – 30Hz
- Amplitude: <25μV
- Mostly on temporal and frontal lobe
- Eyes open, mental activity
- Excitement
II. Basic wave types.
4. What are the characteristics of Gamma wave?
30 – 100Hz
=> short-term memory matching
II. Basic wave types.
5. What are the characteristics of Theta wave?
- Rhythmic, 4 – 7Hz
- Drowsy, sleep
- Parietal and temporal regions in children
- Disappointment and frustration in some adults
II. Basic wave types.
6. What are the characteristics of Delta wave?
- Slow: 0,5 – 4Hz
- Often: voltages 2-4 times greater than other types of waves
- In adults: normal deep sleep rhythm
- May appear during awake state in infants
- If it appears in adults during awake state => brain tumor
III. Origin of EEG waves
1. What is the origin of EEG waves?
- Thousands/millions of cortical neurons firing in synchrony with one another
- Oscillations of EC (‘’field’’) potentials
+) Are more important for EEG signals than APs, because APs are short + fast = do not occur at the same time in different neurons -> cannot be summed (asynchronous)
+) Cellular mechanism of field potentials = alternating EPSPs and IPSPs responsible for the generation of field potentials determine the EEG waves
=> Only dipoles perpendicular to the skull are detected
III. Origin of EEG waves
2. What are the characteristics of Oscillations of EC (‘’field’’) potentials?
- Are more important for EEG signals than APs, because APs are short + fast = do not occur at the same time in different neurons
=> cannot be summed (asynchronous) - Cellular mechanism of field potentials = alternating EPSPs and IPSPs responsible for the generation of field potentials
=> determine the EEG waves
IV. Mechanism of generation of field potentials
1. Describe the mechanism of generation of field potentials
- An ascending excitatory axon will form a synapse with the dendrite of a pyramidal neuron
- Glutamate is released and AMPA-R in the dendrite will open, as a result there will be an influx of positive charges (Na+-influx)
-> local depol. of the dendrite
-> positive charges will move from EC space to the dendrites
-> EC space becomes negative (current sink) - There will be a current within the cytoplasm toward the cell body
-> cell body will become little bit depolarized
-> outward K+-current
-> the EC space around the cell body will become positive and negative inside the soma (current source)
IV. Mechanism of generation of field potentials
2. What are the characteristics of Positive EEG wave?
- Apical IPSP
- Perisomatic EPSP (near soma)
IV. Mechanism of generation of field potentials
3. What are the characteristics of Negative EEG wave?
- Apical EPSP
- Perisomatic IPSP
=> The cellular mechanism cannot be unequivocally determined from the polarity of the EEG wave
IV. Mechanism of generation of field potentials
4A. Only synchronized PSPs induce detectable EEG waves
-> T/F?
True
IV. Mechanism of generation of field potentials
4B. Only synchronized PSPs induce detectable EEG waves
-> Explain
- Individual neurons produce characteristic EPSPs and IPSPs in a synchronized manner
- Under these conditions, the electrical activity form these neurons is summed -> signal strong enough to be detected on the surface
- Thalamus is a very important factor in this synchronization process
V. Describe Mechanisms of synchronizations
- Different neural circuit can oscillate in the same frequency range -> when we detect an EEG wave, we cannot be entirely sure which system caused it
- Example:
+ Thalamic delta rhythm: in deep sleep
+ Cortical delta: surgical removal of the thalamus -> enhancement of neocortical delta
activity
=> Thalamocortical oscillations are important in alpha rhythm
VI. Thalamocortical synchronization
1. Describe Thalamocortical synchronization
- Relay nuclei and the nucleus reticularis thalami are interconnected in the thalamus
- These interconnections may be responsible for the oscillations, which are transmitted to the cortex
- There may also be oscillations between the cortex and relay nuclei, because the cortex will send many fibers back to the thalamus
VI. Thalamocortical synchronization
2. What is network oscillation?
one set of neurons interact with another set of neurons, and the
activity oscillates in these 2 populations
VI. Thalamocortical synchronization
3 What is Recurrent collateral inhibition?
if one neuron population is activated, this activity
(after a delay), will inhibit the same neuron population – inhibitory interneurons are
involved
=> there is an activity followed by an inhibition
VI. Thalamocortical synchronization
4. What is Post-inhibitory rebound?
if the neurons are inhibited for a time period, they will become spontaneously activated after the inhibition disappears
VII. Evoked potentials
1. Describe evoked potentials
- Normal EEG recording => spontaneous potentials
- Evoked potentials => following presentation of a stimulus
- ERP: event-related potentials = time-locked to some ‘’event’’
+ auditory evoked potentials (AEPs): e.g. clicking sound
+ visual evoked potentials (VEPs): e.g. pattern-reversal checkerboard
+ somatosensory evoked potential (SSEPs): e.g. peripheral nerve stimulation
VII. Evoked potentials
2. Give an example of auditory evoked potentials (AEPs)?
clicking sound
VII. Evoked potentials
3. Give an example of visual evoked potentials (VEPs)?
e.g. pattern-reversal checkerboard
VII. Evoked potentials
4. Give an example of somatosensory evoked potential (SSEPs)
peripheral nerve stimulation
VII. Evoked potentials
5. What should happen in order to isolate and visualize these evoked potentials on EEG?
In order to isolate and visualize these evoked potentials on EEG, the stimuli must occur several hundred times during the EEG recording and averaged so that the background noise can be subtracted and the stimuli signal can be isolated.
VIII. Describe Magnetoencephalography (MEG)
- EEG mainly detects the dipoles which are perpendicular to the skull
- However, the cerebral cortex has gyri and sulci
-> the pyramidal neurons in the sulci will produce field potential parallel to the surface of the skull = not well detected by EEG
-> detected by MEG - This change in current flow will generate a magnetic field
-> can be measured - The magnetic field is very low = need a special device to detect the magnetic field changes induced by the current
-> SQUID (superconducting quantum interference device) = a very sensitive magnetometer
IX. Epilepsy
1. What is Epilepsy?
Disease states characterized by behavioral and EEG seizures. Uncontrolled excessive activity of either part or all of the CNS
IX. Epilepsy
2. Give the classification of Epilepsy
- Partial (focal)
- Generalized
IX. Epilepsy
3A. Describe partial (focal)
- Partial (focal): only part of the brain shows abnormal activity
+) Partial simple seizures: consciousness is retained
+_ Partial complex seizures: consciousness is lost
IX. Epilepsy
3B. Give and describe an example of partial simple - Epilepsy
Partial simple: Jacksonian march
- Originates in the motor cortex
- Localized contractions of contralateral muscles
- Spread follows the somatotopic map of the motor cortex
- People are aware of what is occurring during the seizure
IX. Epilepsy
3C. Give and describe an example of partial complex - Epilepsy
Partial complex: psychomotor epilepsy
- Originates in the limbic structures of the temporal lobe
- May cause: short period of amnesia, attack of abnormal rage, sudden anxiety, discomfort/fear, incoherent speech, mumbling of trite phase
IX. Epilepsy
4A. Describe generalized epilepsy
Generalized: large regions of the brain are involved, and consciousness is lost
- Grand mal: tonic/clonic contractions of muscles on both sides of the body (maybe aura, post-seizure depression
- Petit mal: brief loss of consciousness, spike and wave EEG pattern
IX. Epilepsy
4B. Give and describe an example of grand mal
Grand mal: aura, tonic/clonic seizures
- Seconds – 4min
- Bites or ‘’swallows’’ his tongue, cyanosis
- Urination + defecation
- Post-seizure depression (stupor for minutes, sleep for hours)
- Triggers = ethanol, fever
IX. Epilepsy
4C. Give and describe an example of Petit mal
Petit mal: absence epilepsy
- 3 to 30 seconds of unconsciousness
- Maybe twitch-like contractions of muscles – usually in the head region (e.g. blinking of eye)
- Typically appears first during late childhood and then disappears by age 30
- Spike and dome can be recorded over most of the cerebral cortex (involved most of the thalamo-cortical activating system)
X. Sleep
1. Why is sleep a basic requirement?
- We spend about one third of our life in sleep
- About 6-8h/day average requirement in adults
- Sleep is a basic requirement
+) Possible to remain awake voluntarily for only about 3 days
+) After the 4th day, disturbed psychological functions (e.g. visual/auditory hallucinations, memory lapses, impaired moral judgement)
+) Sleep deprivation was used to extract confession
X. Sleep - the circadian rhythm of sleep
2A. What is the circadian rhythm of sleep
- Endogenous rhythm ≈25 hours (?)
- Normally entrained by the light-dark cycle (suprachiasmatic nuclei)
- Jet lag and isolation from the outside world can mess up with the sleep cycle
X. Sleep - the circadian rhythm of sleep
2B. How does blue light participate in the circadian rhythm of sleep?
Blue light triggers melanopsin
-> stimulates retino-hypothalamic tract (non-visual fibers)
-> activates suprachiasmatic nuclei in HT
-> INHIBITS the SYM system
(-> NE is released in the pineal gland
-> release of melatonin)
(hormone of darkness)
- Melatonin causes sleepiness
- Blue light blocks the
production of melatonin = not sleepy
X. Sleep
3. What is the function of sleep?
Sleep is an active process:
- Sleep ≠ loss of consciousness
- Sleep ≠ loss of brain activity
- Actively controlled mechanism
- Characterized by altered responsiveness to environmental stimuli
=> Cortical function is not stopped, but recognized during sleep
X. Sleep - EEG in sleep stages
4A. What are the 4 stages of slow-wave sleep?
A person falling asleep passes through 4 stages of slow- wave sleep, over a period of 30-45 minutes:
NREM (non-rapid eye movement) sleep: (low frequency, high amplitude waves)
- Stage 1: drowsy alpha waves to theta waves
- Stage 2: slow theta waves with small bursts of activity known as sleep spindles (12-14Hz) and K-complexes (large, slow potentials)
- Stage 3: theta waves change to low amplitude delta waves
- Stage 4: delta waves (0,5 – 2Hz), deep sleep/slow wave sleep
=> ANS changes: ↓HR + ↓BP
=> In order to wake up, the person must pass through the sleep stages in reverse
X. Sleep - EEG in sleep stages
4B. What happen in stage 1?
Stage 1: drowsy alpha waves to theta waves
X. Sleep - EEG in sleep stages
4C. What happen in stage 2?
Stage 2: slow theta waves with small bursts of activity known as sleep spindles (12-14Hz) and K-complexes (large, slow potentials)
=> In order to wake up, the person must pass through the sleep stages in reverse
X. Sleep - EEG in sleep stages - 4 stages of slow-wave sleep?
4D. What happen in stage 3?
Stage 3: theta waves change to low amplitude delta waves
X. Sleep - EEG in sleep stages
4E. What happen in stage 4?
Stage 4: delta waves (0,5 – 2Hz), deep sleep/slow wave sleep
X. Sleep - REM sleep
5A. What are the features of REM Sleep?
REM sleep: (high frequency, low amplitude)
- EEG is desynchronized
- Muscle tone is lost, but phasic contractions
occur in some muscle (eye muscles)
- Cause Autonomic changes
- REM sleep varies with age
- Difficult to arouse a person from REM sleep, but internal arousal is common
X. Sleep - REM sleep
5B. What are the autonomic changes caused by REM Sleep?
- Temperature regulation is lost
- HR, BP and respiration changes
- Most dreams occur during REM sleep (good thing muscle tone is lost)
- Penile erection
X. Sleep - REM sleep
5C. How does REM sleep vary with age?
- Newborn: spend about half of their sleep time in REM
- Young adult: 20% to 25% of their sleep is REM sleep
- Elderly have little REM sleep
XI. Ascending arousal system: (AAS)
1. What are the features of Ascending arousal system: (AAS)?
- Nuclei send their axons into the cerebral cortex
diffusely, others to the thalamus - These nuclei provide persistent depolarization = ensures the awake state
- Lesion of the AAS -> somnolence/coma
XII. Hypothalamic control of the arousal system
1. What are the features of Hypothalamic control of the arousal system?
XII. Hypothalamic control of the arousal system
2. What are the features of VLPO (ventrolateral preoptic nucleus)?
- In the lateral hypothalamic area
- Uses GABA and galanin to inhibit the arousal system => VLPO active in sleep
- VLPO lesion => insomnia (cannot go to sleep)
XII. Hypothalamic control of the arousal system
3. What are the features of Orexin (hypocretin)?
- In the lateral hypothalamic area
- Stabilizes the arousal system (awake state)
- Orexin deficiency: narcolepsy
XIII. Sleep/wake cycle regulation: VLPO/arousal system (FLIP-FLOP)
1. What are the features of VLPO/arousal system (FLIP-FLOP)?
Awake:
- Arousal system prevails
- VLPO is inhibited
Sleep:
- VLPO prevails
- Arousal system is inhibited
XIII. Sleep/wake cycle regulation: VLPO/arousal system (FLIP-FLOP)
2. How does VLPO/arousal system (FLIP-FLOP) switch to sleep?
When circadian sleep drive or homeostatic need for sleep become great enough, the flip-flop circuit will suddenly give way and reverse
XIII. Sleep/wake cycle regulation: VLPO/arousal system (FLIP-FLOP)
3. Make a schematic diagram of VLPO/arousal system (FLIP-FLOP)?
XIV. Orexin deficiency: narcolepsy
1. What are the symptoms of Orexin deficiency: narcolepsy?
XV. Learning and memory
1. What is learning?
Learning is a change in the reaction to stimuli, whereas memory is the storage of what has been learned
XV. Learning and memory
2. What are the 2 types of learning/memory?
Learning/memory can be implicit or explicit:
- Implicit: Unconscious, automatic behavior, behaviorally expressed (much as learned reflexes), NOT verbally expressed.
- Explicit: Storage of past life events, can be verbally expressed as feelings or ideas
XV. Learning and memory
3. What is implicit?
Implicit: Unconscious, automatic behavior, behaviorally expressed (much as learned reflexes), NOT verbally expressed.
XV. Learning and memory
4. What is Explicit?
Storage of past life events, can be verbally expressed as feelings or ideas
XV. Learning and memory
5A. What are the 4 main categories of implicit learning?
- Non-associative learning – Reflex pathways
- Associative – (Cerebellum and Amygdala): Entails learning to respond to a previously
- Procedural – (Striatum): Activities learned due to repeated practice
- Priming – (Neocortex): After a clue or trigger, memory retrieval is improved.
XV. Learning and memory - Implicit learning
5B. What are the features of Non-associative learning?
XV. Learning and memory - Implicit learning
5B. What are the features of associative learning?
XV. Learning and memory - Implicit learning
5C. What are the features of procedural learning?
Procedural – (Striatum): Activities learned due to repeated practice
- Learning to play an instrument
XV. Learning and memory - Implicit learning
5D. What are the features of priming learning?
Priming – (Neocortex): After a clue or trigger, memory retrieval is improved.
- A perfume scent that reminds you of a person.
XV. Learning and memory - Explicit memory
6A. What are the features of explicit memory?
XV. Learning and memory - Explicit memory
6B. What happen during encoding of explicit memory?
Aided by attention, motivation, and connection to previous knowledge.
a. Begins in sensory area in pre-frontal part of brain.
XV. Learning and memory - Explicit memory
6C. What happen during consolidation of explicit memory?
Changes in synaptic transmission OR creation of new synapses.
XV. Learning and memory - Explicit memory
6D. What happen during Storage of explicit memory?
- At different parts of the brain depending on short, intermediate, or long-term memory.
- Temporal lobe is important in memory storage process.
- With damage or removal of the temporal lobes, patients still retain their short and long-term memories but cannot store new ones.
- These patients can still learn new procedural tasks such as playing a sport or instrument, even if they do not remember practicing.
XV. Learning and memory - Explicit memory
7. What are the 3 types of Time length of explicit memory?
explicit memory can be short term, intermediate or long-term.
1. Short term – necessary for only a few moments (i.e. instructions)
2. Intermediate – information that can be learned for a few days or so but then forgotten (i.e. anatomy).
3. Long term – difficult to forget (i.e. your family’s names).
XVI. Long-Term Potentiation (LTP):
1. What is Long-Term Potentiation (LTP)?
- Persistent strengthening of synapses based on recent patterns of activity.
- This produces a long-lasting increase in signal transmission between two neurons.
- It is one of several phenomena underlying synaptic plasticity (ability of chemical synapses to change their strength).
- Since memories are thought to be encoded by modifications of synaptic strength, LPT is widely considered one of the major cellular mechanisms that underlies learning and memory.
XVI. Long-Term Potentiation (LTP):
2. What types of receptor does Long-Term Potentiation (LTP) involve?
NMDA receptors
XVI. Long-Term Potentiation (LTP):
3. What is the mechanism of Long-Term Potentiation (LTP) involve?
LTP can increase synaptic strength for hours to days, via the following mechanism:
High frequency stimulation
-> ↑ AMPA-R activity
-> stronger depolarization
-> NMDA-R activation
-> ↑[Ca2+]
-> CAM-Kinase-II activation
-> phosphorylation of AMPA-R
-> ↑AMPA-R activity (new receptors)
=> The synapse has been strengthened with appearance of more AMPA receptors to the postsynaptic membrane
=> It will respond more rapidly and more strongly to future releases of glutamate
