STATES OF CONSCIOUSNESS, SLEEP

Olga Vajnerová

Department of Physiology

2nd Medical School

Charles University Prague

EEG

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

Elektroencephalograf

Elektroencephalogram

apparatus

record

(registration, paper)

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

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

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

Montage

A standard set of placements for EEG electrodes

Pyramidal neuron

Apical dendrite

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

                                                                                     

Evoked Potentials

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

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

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

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

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

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)

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

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

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

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

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)

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

Epilepsy seizure petit mal (absence)

Spike and wave activity

The seizure was clinically manifested as a staring spell

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.

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.

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

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

Ascending arousal system

Ascending arousal system – the most important conections1. 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)

Arousal reaction

1. Sensory signal – all sensory fibers project collaterals to RF and activate AAS

2. Limbic system – alert under the influence of emotions

Arousal – unconsciousness

Quantitative score according to:

behavior of organism

EEG

Eye opening

4 spontaneously

3 to speech

2 to pain

1 non

Motor response

6 obeys commands

5 localises to pain

4 withdraws from pain

3 decorticate (flexion) rigidity

2 decerebrate (extension) rigidity

1 no reaction

Verbal response

5 patient is orientated and converse

4 patient is confused but communicate

3 inappropriate, accidental words, no meaningful conversation

2 incomprihensible sounds, no words

1 no verbal language

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

4 withdraws from pain

3 decorticate (flexion) rigidity

2 decerebrate (extension) rigidity

1 no reaction

Verbal response

5 patient is orientated and converse

4 patient is confused but communicate

3 inappropriate, accidental words, no meaningful conversation

2 incomprihensible sounds, no words

1 no verbal language

Glasgow Coma Scale (GCS)

GCS coma

8 and less heavy coma

9-12 medium

13 and more light

Sleep

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

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

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

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

Polysomnografie

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

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

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)

Sleep disturbances

HypersomniaInsomnia - continuously having difficulty in falling asleep and sleep maintenanceBruxism – involuntary grinding or clenching of the teeth while sleeping

Dyssomnie (parasomnie)

Somnambulismus – sleepwalking – activities without conscious knowledge

Night terror - pavor nocturnus

Night mares

Narkolepsy-cataplexy syndromeSleep attacks which cannot be volitionally avoidedCataplectic attacks (loss of affective tone)