STATES OF CONSCIOUSNESS SLEEP Olga Vajnerov Department of

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

EEG

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 ECo. G and evoked potentials Hans Berger (Swiss psychiatrist) 1929 – human EEG, basic rhythm of electrical activity alfa (8 -13 Hz) and beta (14 -30) After 1945 – EEG as a clinical inspection

Elektroencephalograf apparatus Elektroencephalogram record (registration, paper)

EEG activity is mostly rhytmic and of sinusoidal shape rhythm 14 -30 Hz rhythm 8 -13 Hz (quiet wakefulness) rhythm 4 -7 Hz rhythm 3 and less Hz rhythm , rolandic rhythm 8 -10 Hz

Normal EEG – lokalization of graphoelement types Frontal - activity Fist Unbend fingers parietal – , rolandic rhythm Temporal , activity Eyes open Eyes closed Temporo-parietooccipital - activity Podle Faber Elektroencefalografie

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

Montage A standard set of placements for EEG electrodes

Pyramidal neuron Apical dendrite

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

Evoked Potentials

Average evoked potentials Event-related potentials Routine procedure of clinical EEG laboratories from 1980 s 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

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)

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 1 to 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 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: Retina Rods and Cones Bipolar neurons Ganglion cells Anterior visual pathways Retrochiasmal pathways Optic nerve Optic chiasm Optic tract Lateral geniculate body Optic radiation Occipital lobe, visual cortex

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

VEPs as a tool in the diagnosis of multiple sclerosis: Excessive interocular difference in P 100 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 P 100

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 Eyes open Alpha activity Spike and wave activity Petit mal (absence) Grand mal Tonic phase Temporal seizure = partial seizure with complex symptomatology clonic Theta až delta aktivita Septo-hipocampal system Beta aktivita 15 -20 Hz unconsciousness (coma)

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 – vigilance High level of vigilance = arousal Ability to orient appropriately to stimuli. Dependent on the activity of two cerebral hemispheres.

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

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 C 1) Sleep and wakefulness alternate

Ascending arousal system

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)

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 Glasgow Coma Scale (GCS) 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, meaningful conversation 2 incomprihensible sounds, no words 1 no verbal language no

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

Sleep

Sleep The age-old explanation until 1940 s – sleep is simply a state of reduced activity Nathaniel Kleitman in early 1950 s 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

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: EEG K-complex and sleep spindle 3. Delta activity (slow highamplitude waves) more than 20% 4. Delta activity more than 50% EEG EMG EOG REM – paradoxical sleep EEG Eye movements, EMG loss of muscle tone EOG Podle Faber – materiály k Ph. D

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 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

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