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STATES OF CONSCIOUSNESS, SLEEP
Olga Vajnerová
Department of Physiology
2nd Medical School
Charles University Prague
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Consciousness 2 different concepts
1. Wakefulness
2. Be aware of oneself = self-awareness (thoughts, perception, memories and feelings)
Wakefulness – vigilanceHigh level of vigilance = arousal
Ability to orient appropriately to stimuli. Dependent on the activity of two cerebral hemispheres.
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Wakefulness – vigilance
Sleep AAS activity is decreasedActivity of sleep centers is increased
Can be waken up
Unconsciousness - Generalized impairment of consciousness, diffuse
dysfunction in both cerebral hemispheres
Cannot be waken up
States of consciousness
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EEG
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EEG
Richard Caton 1875 – 1. Registration of ECoG and evoked potentials
Registration of electrical brain potentials measured form tha surface of the scull
It reflects function properties of the brain
Hans Berger (Swiss psychiatrist) 1929 – human EEG, basic rhythm of electrical activity alfa (8-13Hz) and beta (14-30)
After 1945 – EEG as a clinical inspection
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Elektroencephalograf
Elektroencephalogram
apparatus
record
(registration, paper)
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EEG activity is mostly rhytmic and of sinusoidal shape
rhythm 8-13 Hz (quiet wakefulness)
rhythm , rolandic rhythm 8-10 Hz
rhythm 4-7 Hz
rhythm 3 and less Hz
rhythm 14-30 Hz
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Normal EEG – lokalization of graphoelement types
Frontal - activity
parietal – , rolandic rhythm
Temporal - , activity
Temporo-parieto- occipital - activity
Fist Unbend fingers
Eyes open Eyes closed
Podle Faber Elektroencefalografie
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Ontogenesis EEG
Until 1 year – (1-3 Hz) not too regular, high amplitude,
1- 3 years - rhythm (4-7 Hz)
3-5 let – more regular prealfa (6-8 Hz)
5-7 let – regular (8-13Hz) medial voltage,
frontally
Is blocked by eye opening
Very good reactivity
Attenuation by opening eye is imperfect
Is not blocked by eye opening
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Montage
A standard set of placements for EEG electrodes
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Pyramidal neuron
Apical dendrite
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Thalamocortical system (thalamic activity is rhytmic)
Ascending arousal systém (AAS or RAS) pathways from brain stem RF to thalamus
Slow-wave
sleep
Waking
Thalami
c firing
Bursts Single spikes
EEG High voltage
low
frequency
Low voltage
high
frequency
irregular
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Thalamocortical modulation
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Evoked Potentials
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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
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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
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How to reduce the amount of the noise
-Superimposition
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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
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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
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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
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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
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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
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Normal VEP
VEPs to pattern-reversal, full-field stimulation of the right eye
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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
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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
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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
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Epileptic seizures are characterized by following disturbances:
occur in attacks, abrupt onset
usually accompanied by disturbances of consciousness
usually accompanied by disturbances of motor and/or sensory functions and/or vegetative symptoms
abnormal EEG recordings
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Seizures
I. Partial (focal)
a simple partial seizures (without alternation of consciousness)
b complex partial seizures (with impairment of consciousness
c comples partial seizures evolving to secondarily generalized seizures
II. Generalized seizures (simultaneous disruption of normal brain activity in both hemispheres) (convulsive or noncolvulsive)
a absence (petit mal)
b tonic-clonic (grand mal)
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Typical epileptic grafoelements in EEG
Petit mal (absence)
Grand malTonic phase clonic
unconsciousness (coma)
Temporal seizure = partial seizure with complex symptomatology
Septo-hipocampal system
Alpha activity Eyes open
Spike and wave activity
Beta aktivita 15-20 Hz
Theta až delta aktivita
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Epileptic seizure - grand mal
This 40 year-old patient had epilepsy worsened by an inappriopriate change in his antiepileptic treatment.
Seizure begins by a sudden scream with bilateral axial flexion with an internal rotation of both upper limbs.
A slight non-forced rotation of head to the right is then followed by a clonic phase.
A second tonic phase occurs 55 seconds after seizue onset, followed by bilateral clonic jerks, a stertorous breathe.
Post-ictal headache and limb stiffness.
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Sleep
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Ascending arousal system
Frederic Bremer (30. years of 20. century)
Cerveau isolé (intercollicular midbrain transection between colliculi superiores and inferiores)
uncosciouness, EEG of sleep type
Encephal isolé (transection at C1)
Sleep and wakefulness alternate
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Ascending arousal system – the most important conections1. Reticular formation (in the brain stem)
2A. Non-specific thalamic nuclei: intralaminar, periventicular, reticular
2B. Subthalamus a hypothalamus
3. Cerebral cortex (all regions, divergention)
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VigilityReticular ascenden system RAS
Talamocortical synchronization is disturbed
Sleep activity of RAS decreased talamocortikcal
synchronizaction
activity of sleep centers
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Arousal reaction
1. Sensory signal – all sensory fibers project collaterals to RF and activate AAS
2. Limbic system – alert under the influence of emotions
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Sleep
Nathaniel Kleitman in early 1950s made remarkable discovery:
Sleep is not a single process, it has two distinct phases:
REM sleep (paradoxical) is characterized by Rapid Eye Movements
Non-REM sleep (slow-wave sleep)
The age-old explanation until 1940s – sleep is simply a state of reduced activity
Sleep is an actively induced and highly organized brain state with different phases
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Brain correlates of sleep
Non-REM nuclei raphe (serotonin)
ncl. tractus solitarii
cholinergic neurons of RF (pons, mesencefalon)
ncl. reticularis thalami
REM nucleus reticularis pontis oralis, (nucleus of RF at the junction of the pons a midbrain), (higher activity during REM sleep, its destruction eliminates REM sleep)
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Charakteristic of non-REM•Skeletal muscles – relaxed
•Parasympaticus predominate –heart rate, preassure, motility of GIT, breathing
•Dreams – usually no
•Humans are more difficult to awaken in 4. stage
Charakteristic of REM
•Skeletal muscles – loss of tone except eye and breathing muscles•Sympaticus predominate – heart rate, preassure, motility of GIT, breathing, erection in men•Dreams – are frequent•EEG remind wakefulness – for this reason paradoxical
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4 stages of non-REM sleep
1. Slight slowing of EEG Alfa changes into theta
2. Theta activity a grafoelements:
K-complex and sleep spindle
3. Delta activity (slow high-amplitude waves) more than 20%
4. Delta activity more than 50%
REM – paradoxical sleep
Eye movements,
loss of muscle tone
EEG
EMG
EOG
EEG
EMG
EOGPodle Faber – materiály k PhD
EEG
EEG
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Hypnogram
Extensity REM = duration
Intensity REM = fruitfulness (eye movements, jerks)
Selectiv deprivation = REM sleep is blocked
Next night rebound efect
Aggressivenes, memory, hypersexuality, polyphagia
REM is related to psychological activity
Non REM to physical
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Polysomnography
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Sleep in phylogenesis and ontogenesis
Fish – no sleep
Reptiles – begining of non REM
Birds – beginning of REM
Mammalian – developed
non REM – REM cyklus
From 30. week of gravidity – REM
Newborn – REM 50%
Preschool age – REM 30%
Adults – REM 20%
In phylogenesis there is non REM first
In ontogenesis there is REM first
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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
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Thank you for your attention?
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