1. STATES OF CONSCIOUSNESS, SLEEP
Olga Vajnerová
Department of Physiology
2nd Medical School
Charles University Prague

2. EEG

3. EEG
Registration of electrical brain potentials measured form tha surface of the scull
It reflects function properties of the brain
Richard Caton 1875 – 1. Registration of ECoG and evoked potentials
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

4. Elektroencephalograf
Elektroencephalogram
apparatus
record
(registration, paper)

5. EEG activity is mostly rhytmic and of sinusoidal shape
rhythm  Hz
rhythm  8-13 Hz (quiet wakefulness)
rhythm  4-7 Hz
rhythm  3 and less Hz
rhythm , rolandic rhythm 8-10 Hz

6. Normal EEG – lokalization of graphoelement types
Frontal -  activity
Fist
Unbend fingers
parietal – , rolandic rhythm
Temporal - , activity
Eyes open
Eyes closed
Temporo-parieto- occipital -  activity
Podle Faber Elektroencefalografie

7. Until 1 year –  (1-3 Hz) not too regular, high amplitude,
Ontogenesis EEG
Until 1 year –  (1-3 Hz) not too regular, high amplitude,
Is not blocked by eye opening
Attenuation by opening eye is imperfect
1- 3 years - rhythm  (4-7 Hz)
3-5 let – more regular prealfa  (6-8 Hz)
Is blocked by eye opening
5-7 let – regular  (8-13Hz) medial voltage,
frontally 
Very good reactivity

8. Montage
A standard set of placements for EEG electrodes

11. Pyramidal neuron
Apical dendrite

13. Thalamocortical system (thalamic activity is rhytmic) Slow-wave sleep
Waking
Thalamic firing
Bursts
Single spikes
EEG
High voltage low frequency
Low voltage high frequency irregular
Vložit obr Kandel str 899
Ascending arousal systém (AAS or RAS) pathways from brain stem RF to thalamus

14. Evoked Potentials
                                                                                     

15. 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

16. 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

17. How to reduce the amount of the noise
Superimposition

18. How to reduce the amount of the noise
Simplified diagram illustrating how coherent averaging enhances a low level signal (coherent = EP time locked to the evoking stimulus)

19. 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

20. 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

21. 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

22. 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 tests at least to ensure that the waveforms are replicable

23. Normal VEP
VEPs to pattern-reversal, full-field stimulation of the right eye

24. Visual-evoked potentials (VEP)
Electrical activity induced in visual cortex by light stimuli
Retina
Rods and Cones
Anatomical basis of the VEP:
Bipolar neurons
Ganglion cells
Anterior visual pathways
Optic nerve
Optic chiasm
Optic tract
Lateral geniculate body
Retrochiasmal pathways
Optic radiation
Occipital lobe, visual cortex

25. 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

26. VEPs as a tool in the diagnosis
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

27. 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

28. 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)

29. Typical epileptic grafoelements in EEG
Eyes open
Alpha activity
Petit mal (absence)
Spike and wave activity
unconsciousness (coma)
clonic
Tonic phase
Grand mal
Temporal seizure = partial seizure with complex symptomatology
Septo-hipocampal system
Theta až delta aktivita
Beta aktivita Hz

30. Epilepsy seizure petit mal (absence)
Spike and wave activity
The seizure was clinically manifested as a staring spell

31. 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.

32. Consciousness 2 different concepts
1. Wakefulness
2. Be aware of oneself = self-awareness (thoughts, perception, memories and feelings)
Wakefulness – vigilance
High level of vigilance = arousal
Ability to orient appropriately to stimuli. Dependent on the activity of two cerebral hemispheres.

33. States of consciousness
Wakefulness – vigilance
Sleep AAS activity is decreased
Activity of sleep centers is increased
Can be waken up
Unconsciousness - Generalized impairment of consciousness, diffuse dysfunction in both cerebral hemispheres
Cannot be waken up

34. 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

35. Ascending arousal system

36. Ascending arousal system – the most important conections
1. Reticular formation (in the brain stem)
2. A. Non-specific thalamic nuclei intralaminar
periventicular
reticular
B. Subthalamus a hypothalamus
3. Cerebral cortex (all regions, divergention)

37. Arousal reaction
Sensory signal – all sensory fibers project collaterals to RF and activate AAS
Limbic system – alert under the influence of emotions

38. Arousal – unconsciousness
Quantitative score according to:
behavior of organism
EEG

39. Glasgow Coma Scale (GCS)
Eye opening 4
spontaneously 3
to speech 2
to pain 1
non
Motor response 6
obeys commands 5
localises to pain
withdraws from pain
decorticate (flexion) rigidity
decerebrate (extension) rigidity
no reaction
Verbal response
patient is orientated and converse
patient is confused but communicate
inappropriate, accidental words, no meaningful conversation
incomprihensible sounds, no words
no verbal language
Glasgow Coma Scale (GCS)
GCS
coma
8 and less
heavy coma
9-12
edium
13 and more
light

40. Glasgow Coma Scale (GCS)
Eye opening 4
spontaneously 3
to speech 2
to pain 1
non
Motor response 6
obeys commands 5
localises to pain
withdraws from pain
decorticate (flexion) rigidity
decerebrate (extension) rigidity
no reaction
Verbal response
patient is orientated and converse
patient is confused but communicate
inappropriate, accidental words, no meaningful conversation
incomprihensible sounds, no words
no verbal language
Glasgow Coma Scale (GCS)
GCS
coma
8 and less
heavy coma
9-12
medium
13 and more
light

41. Sleep

42. Sleep
The age-old explanation until 1940s – sleep is simply a state of reduced activity
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)
Sleep is an actively induced and highly organized brain state with different phases

43. Charakteristic of non-REM
Skeletal muscles – relaxed
Parasympaticus predominate –
Dreams – usually no
Humans are more difficult to awaken in 4. stage
Charakteristic of REM
Skeletal muscles – loss of tone except eye and breathing
Sympaticus predominate – heart rate, preassure, motility of GIT, breathing, erection in men
Dreams – are frequent
EEG remind wakefulness – for this reason paradoxical

44. 4 stages of non-REM sleep
EEG
1. Slight slowing of EEG Alfa changes into theta
EEG
2. Theta activity a grafoelements:
K-complex and sleep spindle
EEG
3. Delta activity (slow high-amplitude waves) more than 20%
4. Delta activity more than 50%
EMG
EOG
REM – paradoxical sleep
Eye movements,
loss of muscle tone
EEG
EMG
EOG
Podle Faber – materiály k PhD

45. Extensity REMu = duration
Hypnogram
Extensity REMu = duration
Intensity REMu = 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

46. Polysomnografie

47. 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

48. 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

49. 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)

50. Dyssomnie (parasomnie)
Sleep disturbances
Hypersomnia
Insomnia - continuously having difficulty in falling asleep and sleep maintenance
Bruxism – involuntary grinding or clenching of the teeth while sleeping
Dyssomnie (parasomnie)
Somnambulismus – sleepwalking – activities without conscious knowledge
Night terror - pavor nocturnus
Night mares
A night terror, also known as pavor nocturnus, is a parasomnia disorder characterized by extreme terror and a temporary inability to regain full consciousness. The subject wakes abruptly from slow-wave sleep, with waking usually accompanied by gasping, moaning, or screaming. It is often impossible to fully awaken the person, and after the episode the subject normally settles back to sleep without waking. A night terror can rarely be recalled by the subject. They typically occur during non-rapid eye movement
A nightmare is a dream which causes a strong unpleasant emotional response from the sleeper, typically fear or horror

51. Narkolepsy-cataplexy syndrome
Sleep attacks which cannot be volitionally avoided
Cataplectic attacks (loss of affective tone)