EEG and some applications (seizures and sleep)

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EEG and some applications (seizures and sleep) EEG: stands for electroencephalography and is a graphed representation of the electrical activity of the brain. EEG is the recording of electrical activity of the brain especially in the superficial layers i.e. the dendrites of pyramidal cell, by placing the electrodes on the scalp. EEG doesn t record the action potential of one neuron, it rather records the brain electrical activity generated by a group of neurons; it detects the current flow in a wide area. In other words we record the movement of electrons but not the AP from one neuron. In previously mentioned experiments done on primates such as monkeys, recording of an action potential from one neuron was possible, but here since we record EEG using electrodes placed on the skull; many isolating layers such as skin and bone prevent and diminish our ability to record anything. If an electrode was placed in the brain an action potential will be recorded and something like EEG will be recorded called local field. *Reminder: the action potential occurs through ion movement from outside the cell to the inside and vice versa which is similar to current movement that we record as EEG. We place the electrodes at the base of the skull (the distribution is not imp as the Dr mentioned)

EEG recordings differ according to the lobe, the state (asleep or awake), function and dominance of the lobe Brain waves that are detected are differentiated or classified according to their frequency or amplitude. So we classify the waves into ALPHA, BETA, THETA, & DELTA (the Dr said that recording the rate of occurrence of these waves is better than measuring their amplitude) EEG different waves: Wave type Frequency State of detection Extra notes Wave 1 Delta 1-3 Hz -Deep, dreamless sleep -Not moving -Not attentive Slow waves Drowsiness/ early SWS Wave 2 Theta 4-8 Hz -State between wakefulness and sleep Drowsy -Meditation, internal focus, and prayer -Subconsciousness. Drowsiness/ early SWS Wave 3 Alpha 8-13 Hz -Relaxing -Watching television, -Light reading(novel) -Eyes closed. Wave 4 Beta 12-35Hz The normal dominant rhythm: -Thinking -Concentrating -Solving a problem -Making a decision -Judging Occurs in parietal and occipital lobes RELAXED Wakeful Occurs in temporal and frontal lobes INTENSE mental activity

While looking at the EEG you won t be able to differentiate between the different waves. EEG is mainly important in the cases of seizures and epilepsy Now let s talk about SEIZURES Seizures are abnormal electrical activities that we detect in the EEG as a result of an imbalance between excitation and inhibition, it may be described as synchronization of waves Seizures may or may not have a motor effect it depends on the area where the occurred. If a motor effect occurred we call it a Convulsion and it may be tonic or clonic. Seizures and/or convulsions can be acute and isolated however when seizures/convulsions are chronic and are of undefined origin we call it Epilepsy Causes of Seizures: -Idiopathic or 1ry: the reason of occurrence is not known. -Secondary: due to trauma, tumor or any other reason that may influence the excitation/inhibition ratio such as infections, electrolyte imbalance or a raise in the body temperature Seizures may be classified in two ways: First.. According to manifestations ((Generalized Seizure Disorders)) 1) Absence: almost no effect is observed, a brief distraction for 10-30 seconds. And the pt wouldn t know he is having a seizure. Although it may have a simple motor effect like hand shaking or blinking 2) Myoclonic 3) Clonic

4) Tonic-Clonic: also called the grand mal epilepsy. Where spasm and movements occur and then the pt passes out (completely relaxed) 5) Atonic : the pt will simply pass out **Please check the slides for Normal vs Absence and Normal vs Tonic- Clonic EEG recordings** Second.. According to degree of spreading ((Partial Seizure Disorders)) Focal, localized seizures including... - Simple No impairment of consciousness. -Complex Consciousness impaired or disturbed. -Secondarily generalized A focal seizure may spread in the same hemisphere and through the corpus callosum to the other hemisphere due to trauma and it this develops into a generalized seizure (Seizure Spread) (overlap) Keep in mind that seizures occur due to an imbalance between the excitation/inhibition ratio, so a seizure is a result of a misbalanced GLUTAMATE/GABA ratio since glutamate is the main excitatory neuron and GABA is the main inhibitory one. That s why many anticonvulsant drugs work on GABA production, degradation and modulation. Glutamate is a bit harder to work on. Seizures may also be a result of altered ionic conductance (increased excitability) so we also find other anticonvulsant drugs working on the Na or Ca channels

Time to talk about Sleep.. Why do we sleep? Why is it important for us to sleep? Many theories are being discussed: -Adaptive Evolutionary Function -Restorative Function -Brain Plasticity (enhances synaptic connections, memory consolidation) Brain Plasticity is the most accepted theory nowadays Verification of the last theory came from experiments that were done on sleep deprived patients, memory and cognition were affected. In addition many animals died after not sleeping for several days So, sleep occurs actively not passively, it occurs from the brain not from the outside. The brain wants us to sleep in order for it to fix itself. The measurement of hormones in the study of sleep is not accurate except for certain hormones that have receptors in the brain for example the hormone cortisol Sleep is an important mechanism for the brain, so some neurotransmitters have a stimulatory while others have an inhibitory effect on it. Ach, Dopamine, Serotonin, Histamine, and NE cause wakefulness of the brain by activating the reticular activating system resulting in the awake state. Over activation of these NT receptors may lead to insomnia On the other hand, GABA which is produced from the basolateral nucleus in the hypothalamus base of the brain under the hypothalamus results in inhibition of the reticular activating system causing sleep. Over activation of GABA receptors may lead to narcolepsy A newly discovered protein called Hypocretin protein(orexin) is also involved in wakefulness. It activates the awakening center in the brain (containing ach, dopamine,..) thus opposing the GABA transmitter (induces waking up system).

The doctor mentioned that there is a ventral and a dorsal pathway of ascending reticular activating system. The dorsal pathway originates in the pontine and midbrain reticular formation and project to the thalamus which diffusely innervate many areas of the cerebral cortex. The ventral pathway has the same origin but instead of projecting to the thalamus it projects to the hypothalamus and basal forebrain and finally reaches the cortex. Serotonin Paradox: -A depressed patient (low serotonin) may sleep more or may sleep less. -An increase or decrease in serotonin may cause insomnia Even in the 21st century, sleep is not fully understood. However, serotonin plays a definite role in sleep cycles. We can say that high levels of serotonin are associated with wakefulness and low levels with sleep Melatonin melanopsin-expressing retinal ganglion cells stimulate the suprachiasmatic nucleus stimulating paraventricular nucleus with excite the pineal gland to produce melatonin from serotonin as shown in the figure. Melatonin is not considered an inhibitory or stimulatory agent for sleep. However it works as a regulator to the circadian rhythm of sleep. And this is proved by removal of

a suprachiasmatic nucleus from a rat leading to disturbed rhythm of sleep although sleep hours stayed the same (insomnia). A person who sleeps 6 discontinuous hours throughout the day has insomnia however a person sleeping 6 continuous hours at night doesn t have insomnia. *same sleeping hours but different distribution* Insomnia doesn t necessarily mean that we didn t sleep for enough hours it may mean a difficulty in falling asleep or to wake up frequently. Insomnia should be treated since we need sleep for many reasons as mentioned before and a decrease in sleep may lead to memory and cognitive disturbances, However we may say that an increase in melatonin induces sleep and its decrease induces waking up. But a great increase in melatonin may also cause waking up. (paradox) Melatonin tends to decrease with age and that explains why infants sleep more in contrast to adults and old people who tend to sleep less. Adenosine Adenosine causes sleep but how? In the case of work and effort adenosine increases in the body due to increased ATP consumption, so the adenosine binds to A1 receptors on ach neurons and thus preventing the wakefulness state. Caffeine (coffee and tea) act as A1 antagonists, they inhibit the binding of adenosine to these receptors and thus prevent sleeping In some people caffeine has no effect why? This depends on the receptors, the affinity of the caffeine to the receptors, the amount of caffeine and even the presence of caffeine (tolerance)

The stages of sleep : Awake Non-rapid eye movement sleep (NREM) or slow wave sleep and consists of: Stage 1, stage 2, stage 3, stage 4 Rapid eye movement sleep (REM) NREM sleep: Stage 1 : Eyes are closed and relaxation begins; the EEG shows alpha waves; one can be easily aroused Stage 2 : EEG pattern is irregular with sleep spindles (high-voltage wave bursts); arousal is more difficult. Heart rate and blood pressure and muscle tone are normal but some relaxation might occur Stage 3 : sleep deepens;; theta and delta waves appear vital signs (heart rate and breathing)decline and muscle tone decreases dreaming is common Stage 4 : EEG pattern is dominated by delta waves; skeletal muscles are completely relaxed; arousal is difficult A bit of dreaming happens here as well. 70% of bed wetting and sleep walking Normally, we don t pass through all stages of sleep but after stage four we go into the rapid eye movement stage where the brain increases its activity and rapid eye movement occurs

REM sleep Presence of beta activity (desynchronized EEG pattern); brain works just as the waking state, the eyes are rapidly moving while they are closed, the occulomotor is functioning well but the eye muscles are completely paralyzed Physiological arousal threshold increases Heart-rate quickens Breathing more irregular and rapid Brainwave activity resembles wakefulness Genital arousal Loss of muscle tone (paralysis) Vivid, emotional dreams May be involved in memory consolidation Bed wetting may occur, although 70% of bed wetting occurs in stage 4 We actually sleep to reach the REM sleep. REM sleep depends on age (infants have a longer REM sleep) and how tired the person is (the more tired the more REM sleep) During the normal sleep of human three to five cycles occur. A sleep cycle is from the beginning of sleeping till the end of REM sleeping. The first cycle lasts 2-3 hours and the REM stage lasts about 20-30 minutes

Dreams occur in both REM and NREM sleep but with some differences: REM NREM (mainly stage 3, +4) Vivid and exciting ~3 per night Just thinking Longer and more detailed Shorter and less active Fantasy and nightmares Logical and realistic Which dreams do we remember, those happening in REM or NREM? It doesn t differ, it only depends on the blood supply of the brain Sleep disorders: insomnia sleep walking, talking, and eating nightmares and night terrors narcolepsy sleep apnea Good luck Lana Daoud..