Sleep and Consciousness

October 26, 2018 | Author: Std Dlshsi | Category: Thalamus, Science, Sleep, Rapid Eye Movement Sleep, Cerebral Cortex
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SUBJECT: PHYSIOLOGY  TOPIC: SLEEP AND WAKEFULNESS LECTURER: DR. SIMBULAN DATE: MARCH 2011

I. RETICULAR RAS

FORMATION

RETICULAR FORMATION •



thalamic nuclei, and from there projec projects ts diffus diffusely ely to the whole whole cortex.

&

Occupies the midventral portion of the medulla and midbrain Made up of various neural clusters and fibers with distinct functions . Some of  these are: o Cell Cell bodi bodies es whic which h are are serotonergic, noradrenergic, adrenergic o Areas Areas concerned concerned with the regula regulatio tion n of heart heart rate, rate, blood blood pressure, respiration o Some descendi descending ng fibers fibers which which inhibit inhibit transmi transmissio ssion n in sensory sensory pathways in the spinal cord o Areas concerned with spasticity and adjustment of stretch reflexes Concerned with consciousness consciousness o and sleep

II. THE THALAMUS & CEREBRAL CORTEX THALAMOCORTICAL OSCILLATIONS •









RETICULAR ACTIVATING SYSTEM AKA “Ascendin “Ascending g Arousal Arousal System” System” (Kandel) (Kandel)/  /  “Ascending Reticular Activating System”  (Guyton •

• •







A part of the reticular formation which is concerned concerned with consciou consciousnes sness s and sleep A polysynaptic pathway Afferents may come from long ascendin ascending g sensory sensory tracts, tracts, trigemin trigeminal, al, auditory, visual systems, olfactory system. Destroys Destroys the principl principle e on “modality  specificity” o It is “Non-specific” in such a way way that that it can can be acti activa vate ted d with various sensory stimulation Produc Produces es consc consciou ious, s, alert alert state state that that makes perception possible. Pathway:

Reciprocal oscillating activity between the midline thalamic nuclei and cerebral cortex. Refers to the Electrical activity of  neurons with axonal projections to the cortex. Influence the behaviour of the 6layered cortical neurons. What we see in the EEG is basically a summed summed up integrat integrated ed synaptic synaptic activity of the cortical neurons in the 6-layered neocortex. Influenced by signals coming from: o Specific thalamic relay nuclei o Midlin Midline e and intral intralam amina inarr thalamic nuclei.

2 types of activities of thalamocortical neur neuron ons s whic which h play play a role role in arou arousa sall and sleep: •



Phasic (Burst mode) o 0.5 to 4 Hz o Happens Happens during during slow-wave slow-wave sleep (stage 3 & 4 in REM phase) o Within the Delta frequency sleep Transmission (Tonic mode) o 30 to 80 Hz (typically 40 Hz) o Happens during wakefulness and also in REM sleep During SlowWave Sleep Thalamic neur neuron ons s are are

During aware state Thalamic neur neuron ons s are are

produce arousal

Any part of pial surface of  the brain o An electr electrode ode which which is direct directly ly over the primary receiving area for a partic particula ularr sense sense yields yields a surface positive (+) wave o The surface positive wave is followed followed by a small small negative negative wave After a negative wave, the cycle o shall repeat. Primary evoked potential o 1st positive-n positive-negati egative ve wave sequence o Highly specific in its location o Can be observed only where the pathways from a particular sense organ end o From From any any of the primary primary sensory areas depending on specific specific pathway pathway activated activated;; specific specific ascendin ascending g pathway pathway to thalamic relay nuclei specific cortical receiving area (specific area of parietal or occipital cortex) 

So theref therefor ore, e, activity in the thalamocortical oscillations prevents cortical neuro neurons ns from from rece receiv ivin ing g or processing specific inputs. •





Figure 2. This is a slide from Doc Simbulan’s lecture which shows the sleeping cycle of a normal patient. In the 1 st stage, the aler alertt wake wakefu fuln lnes ess s stag stage, e, ther there e is a toni tonic c mode of activity in the thalamus as well as it exhibits Beta waves in the EEG of Cortical areas. It is followed by the relaxed wakefulness stage which also exhibits a tonic mode of activity in the thalamus, but manifests alpha waves when viewed in the EEG of cortical areas. When the patient approaches the NREM sleep, there is a burst mode of activity, with slow waves in the EEG of cortical areas. As it enters the REM sleep, it goes back again to the tonic mode, also with Beta-like waves.

III. EVOKED POTENTIALS •



Diffuse secondary response o 2nd positive-n positive-negati egative ve wave sequence o Picked up from any part of the pial pial surf surfac ace e of the the cere cerebr brum um;; even on top of the sensory cortex itself  o From most of cortica corticall Surface; Surface; activa activatio tion n of non-sp non-speci ecific fic Ascending pathway; nonspecific ascending ascending pathway pathway (enters (enters brainstem reticular formation) enters enters intralam intralaminar inar thalamic thalamic n. and diffusely projects to the whole of neocortex.

CORTICAL

Assesses Asses ses the the integr integrity ity of ascen ascendin ding g pathways. Monito Monitors rs the electr electrica icall events events happenin happening g in the cortex upon stimulation of a sense organ

Figure 3. Primary evoked potential (A) and

projections along with it. They found out that despite the transection, there there are still still signal signals s whic which h can be picked up. o CONCLUSION: Sign Signal als s do not not come come  from from hori horiz zonta ontal  l  connections from the different layer of the from neocortex, neocortex, but subcortical structures It is a mani manife fest stat atio ion n of   activity of neocortical neurons in response to the sig signal nals s comin coming g from from non-speci non-specific fic ascending ascending path pathwa way y from from the the brai brain n arousal system Flash of light  Lateral geniculate nucl nuclei ei funn funnel els s signals from the brainstem (reticular formation), which proje projects cts to the different parts of  the neocor neocortex tex and to the intralaminar midline nuclei. So the source of  sign signal als s whic which h activ activate ate diffu diffuse se secondary respo espon nse are diffused projecti projections ons from brainstem arousal system

















Very minute voltages (microvolt) which are amplified. Various filters cut down certain high frequency and low frequency frequency signal to see the different different activi activitie ties s which which are going going on in the surface of the brain. Record of the variations in brain potential Can be recorded with scalp electrodes thro throug ugh h the the unop unopen ened ed skil skilll or with with electrode on or in the brain. Electrocorticogram (EGoG) is used for the record obtained with electrodes on the pial surface of the cortex EEG records may be bipolar or unipolar o Bipolar: Shows Shows fluctuati fluctuations ons in  potent potential ial betwee between n 2 cortical electrodes o Unipolar: Show potential  differences between a corti cortical cal electr electrode ode and a theoretically indifferent electrode on some part of  the body distant from the cortex “BAT-D-B” sleeping sequence for adults o Beta Beta waves waves of wakef wakefuln ulness ess  Alpha waves  Theta waves  Delta waves in REM

Clinical Significance of Evoked Cortical Potential  To test the integrity of specific sensory pathway of infants, psychiatric patients, and uncooperative or  (1)before ALERT unconscious patients. (Useful especially the WAKEFULNESS: advent of MRI)

IV. ELECTROENCEPHALOGRAM (EEG (EEG); ); SLEE SLEEP P WAVE WAVES S DURI DURING NG STAGES OF SLEEP CHARACTERISTICS OF SLEEP: • •





Humans sleep in a recumbent posture We have a raised threshold to sensory stimulation There is a low level of motor output during sleeping Entails Entails a unique unique behaviour behaviour which we

• • •



14 to 30 Hz Lower amplitude Frontal Frontal region region and over other region during intense mental activity Alpha block o Transition state from alpha rhythm to beta rhythm o “Aro “Arous usal al or aler alerti ting ng response” o “Prehabituation”

o

Alerting a relaxed subject results in the desynchronization of the EEG, with reduction in the alpha activity and increase in beta activity

• •

4 to 7 Hz K complexes and Sleep spindles also appear in stage 2 NREM sleep.

(4) (4) NR NREM EM SLEE SLEEP/ P/ SLOW SLOW WAVE WAVE SLEE SLEEP P (STAGE 3&4):

(2) RELAXED WAKEFULNESS:

• • •

8 to 13 Hz Drowsy, with eyes closed Parietal and occipital sites

• •

0.5 Hz to 4 Hz Dominant during late slow wave sleep

(5) REM SLEEP (PARADOXIACAL SLEEP):

(3) NREM SLEEP (STAGE 1 &2):



Wave similar to wakefulness

THE SCIENCE OF SLEEP •





Unconsciousness from which the person can be aroused by sensory or other stimuli. Sleep vs. Coma o Unconscious patient cannot respond or get aroused to different stimuli 2 stages of sleep that alternate with each other o Slow-wave sleep (“Dreamless Sleep”) Strong, low frequency of   brainwaves Deep, restful sleep (1 st  hour of sleep after being awake for the whole day) Stage where most sleep  is. Characterized when a  pers person on who who was was awak awake e for more than 24 hours hours falls into deep sleep during the 1st hour after going to sleep Progressive slowing of   brainwav brainwaves es arising arising from well-described thalamocortical thalamocortical events. Has 4 stages  Stage 1 Stage 2 Stage 3 Stage 4 • • • •

o

Rapid Rapid eye-move eye-movement ment sleep sleep (“Pa (“Para rado doxi xic cal Sleep leep// Desynchronized Sleep”) Fast, low-voltage activity  Eyes Eyes underg undergo o rapid rapid  movem movement ents s despit despite e the fact the person person is still still asleep 25% of sleep time in  young adults Recurs every 90 minutes 

 

Not so restful – associated with vivid dreaming Paradox that a person can still be asleep despite marked brain activity

Non-R on-REM EM Slee Sleep p

REM RE M slee sleep p

“Dreamle “Dreamless ss Sleep”/ Sleep”/ “Slow-wave Sleep”

“Paradoxical Sleep”/“Desynchronize d Sleep”

Occurs at the first 1 ½ hour of sleep

Appear Appe ars s afte afterr end end of  Non-RE -REM Sleep (Appears every 90 minutes)

Will only last for 5 to 30 minutes Decrease in peri periph pher eral al and and vascular tone (10 to 30% decrease in BP, RR, BMR)

Muscle tone in the body is exceedingly depressed (Strong inhibition of spinal muscle control areas)

Increased neuroendocrine activity (GH and sexual maturation horm hormon ones es from from pituitary is maximal during sleep

Irregular heart and respiratory (Chara (Characte cteris ristic tic dream state)

rate rate of 

Irre Irregu gula larr musc muscle le contractions occur Rapid movement

eyeball

Highly active brain Penile high highly ly clitoris Dreams

are

Dreams

erection and engo engorg rged ed

are

forgotten

remembered

Stage tage were ere a person will be hard to be woken up

Stage where a person will easily be woken up

More difficult difficult in arous arousing ing people people with sensory stimulus Return Return rapidly

to

sleep sleep

V. FURTHER DESCRIPTION OF SLEEP PHASES; DISTRIBUTION OF SLEEP STAGES During the night (Early adulthood) The NREM and REM Phases alternate throughout sleep 4- 6 times, at intervals of 90 minutes. 1) NREM period – A youn young g adul adultt ente enters rs NREM NREM slee sleep, p, pass passes es through stages 1 and 2, and spends 70-100 minutes in stages 3 and 4. 2) REM period follows – The time period of REM ranges from 2 – 10 minutes, shorter at first, but becomes longer in the latter part of the sleep cycle. (There are about 4-6 REM periods per night). From Infants to Adults •

Gamma oscillations at 30–80 Hz are often seen when an individual is aroused  and focuses attention on something. This is often replaced by irregular fast activity  as the individual initiates motor activity in

AS A CHILD DEVELOPS, SLEEP GRADUALLY BECOMES RESTRICTED TO THE NIGHT .

The The dark dark port portio ion n conn connot otes es the the numb number er of  sleeping sleeping hours while the while while the number of  portion is for the number of waking hours. Polyphasi Polyphasic c (multiph (multiphase) ase) sleep sleep followin following g birth birth change changes s first first to biphas biphasic ic (two-p (two-phas hase) e) sleep sleep among preschool children and later to monophasic (single-phase) sleep. Among the elderly, periods of sleep during the day

becomes more frequent again. Kaya may siesta tayo dati nung preschool.   So para parang ng haba habang ng tumatanda tayo, bumabalik tayo sa pagka“infant” uli. •



REM sleep occupies 80% of total sleep per night in premature infants(no figure), and 50 % in a full-term newbor newborn n infant infant Therea Thereafte fterr the proporti proportion on of REM sleep falls falls rapidly rapidly and plateaus at about 20 – 25% Children have more total sleep time and stage 4 sleep than adults

o

EMG

Electro-myography For muscle tone  The reco ecord is the the  electromyogram Body temperature and other autonomic param paramete eters rs are are also also measur measured ed if the perso person n is awake awake,, and in the differ different ent stag stages es of slee sleep p such such as hear heartt rate rate,, respiration and penile erection. Comparing NREM & REM THROUGH POLYSOMNOGRAPHY: 





Parame ter EEG

EOG EMG

NREM

REM

Progressive Fast, low voltage slowing slowing of  activity brain waves Rapid eye movements Muscle atonia with intermittent muscle twitches Fluctuating HR BP shoots up Many stroke cases occur in this stage of sleep Fluctuating RR

• •



REM sleep plateaus from 3 y/o. Boxed numbers/values highlighted  shows the percentage of REM Sleep 20% of sleep is REM!! REM !!

POLYSOMNOGRAPHY  Measures the sleep state through: o EEG Electroencephalography  For cortical activity  The The reco record rd is the the  encephalogram o EOG Electro-oculography  For eye movements  The record is through the  electro-oculogram •

Tongue (2⁰ +++ ++ + respiratory muscle) Intercos Intercostals tals (1⁰ +++ ++ + respiratory muscle) Diaphragm ( 1⁰ +++ ++ ++ respiratory muscle) Plus sign denotes more muscle tone Pababa nang pababa ang muscle tone – • lowest sa REM for tongue and  intercostals. Diaphr Diaphragm agm musc muscle le stays stays the same same so • as to avoid respiratory arrest Lowest ang muscle tone sa REM sleep • especially the tongue. The tongue and genioglossus muscles can lose muscle tone and help obstruct airway passage that could cause restlessness, so when wake up, we feel tired. •

EFFECT EFFE CTS S OF SLEE SLEEP P ON MUSC MUSCLE LES S OF RESPIRATION: 1. Wakefu Wakefulne lness ss exerts exerts a tonic tonic stimu stimulat lating ing effect on motoneurones 2. This This sti stimu mulat lating ing non-RE non-REM M sleep sleep (via (via primary effect of decrea decrease se activa activatio tion n muscles.

effect effect is withdr withdraw awn n in disfac dis facili ilitat tation ion), ), so the non-REM sleep is to of moton motoneur eurone ones s and

3.) Motoneurone activity is generally decrea decreased sed in REM REM sleep sleep.. This This takes takes place place through processes of inhibition and further dis-facilitation.

VI. PHYSIOLOGICAL BASIS OF EEG, EEG, CONSCI CONSCIOUS OUSNES NESS S AND SLEEP •







4.) Similar processes may occur at respirat respiratory ory motoneuro motoneurones nes that drive drive respiratory muscles. •

Awak  NRE e M

RE M



EEG is brough broughtt about about by integ integra rated ted summated activity of synaptic potential of variou various s neoco neocorti rtical cal neuron neurons s especially the pyramidal cell The surface EEG reflects the activity of cortical neurons close to the EEG electrode. High-frequency stimulation of the brainstem reticular formation which “desynchronizes” the EEG. It produces the waves we see . Desynchronizing mechanism o Mechan Mechanism isms s which which produc produce e the low-ampl low-amplitude itude,, fast irregula irregularr Beta-waves of wakefulness o Neural basis of arousal: RAS activity The activity of RAS is the neuronal basis of EEG midbrain tegmentum Lesion Lesion in disrupts the reticular activating system,

RAS. RAS. This This result results s in COMA for long long periods. o COMA has a synchronized wave pattern, with a characteristic slow-wave. Sort Sort of simi simila larr to slow slow wave wave o sleep

fashion. The EEG of such animals is typically low voltage and fast, desynchronized  a pattern typical of waking. In addition, lesions of the lateral and superior portions of the midbrain midbrain that interrup interruptt the medial medial lemni lemnisc scii and other other ascending ascending specific specific sensory sensory leaving ng behin behind d the systems (leavi reticular core intact) fail to prevent the EEG arousal to sensory stimulation .



Figure Figure B. RAS damaged, therefore EEG arousal does not take place, and comatose situatio situation n develops, develops, character characterized ized by slowslowwaves. •

Figure A. RAS still intact, thus EEG arousal intact. o

Large lesions of lower brain stem stem isolat isolating ing the brain brain from from incom incoming ing senso sensory ry signa signals ls thro throug ugh h the the sp spin inal al cord cord in a preparation called: ENCEPHALE ISOLE’ does not result in coma. Animals with this lesion are awake, respond to trigeminal sensory (CN V) as well as visual and auditory cues, and move their faces and eyes in a normal

Effect of RAS Stimulation on Cortical Neurons: RAS activation inhibits burst activity of thalamocortical cortical neurons neurons (which (which occurs occurs during during slow-wave slow-wave sleep). sleep). Detailed Detailed discussi discussion on omitted here. These results in the lowvoltage, irregular fast waves of  wakefulness. Arou Arousa sall Foll Fo llow owin ing g Cort Cortic ical al Stimulation: Thoughts Thoughts and emotions emotions (intra-cortical signals) also increase activity of RAS, and EEG arousal, through through corticof corticofugal ugal fibers fibers descendi descending ng brainstem brainstem reticular reticular to the formation. This This corti cortico cofug fugal al pathwa pathway y to the brainstem reticular formation can keep us awake.



NEURAL NEURAL SUBSTRA SUBSTRATES TES & CREATION CREATION OF SLOW-WAVE SLEEP (NREM SLEEP) •



Slow Slow wave wave slee sleep p can can be prod produc uced ed experimentally by stimulating 3 subcortical “synchronizing” regions below: o Diencephalic sleep zone o Medullary synchronizing zone o Basal foreign sleep zone The natural development of slowwave wave slee sleep p in a huma human n su sub bject ject or experimental mammal can arise from: o In part, absence of  desy desync nchr hron oniz ized ed acti activi vity ty transmit transmitted ted via the ascendin ascending g reticula reticularr system. system. Meaning, Meaning, absence of arousing sensory inputs from the environment, or from the cortex (lack of  worrying worrying or exciting exciting thoughts thoughts// memories) which descend to excite the brainstem ascending reticular system in the reticular formation. o Actively produced by the three “syn “synch chro roni nizi zing ng regi region ons” s” mentioned above, and shown in figure below:

Nucle Nucleii in Pontin Pontine e Retic Re ticula ular r Formation – triggers REM sleep mechanism. (PGO spikes, pontogeniculo-occipital geniculo-occipital spikes, characteristic characteristic of REM sleep, sleep, origi originat nate e in the the latera laterall pontine tegmentum). Below is a neuronal mechanism of REM sleep originati originating ng from the pontine pontine reticula reticularr formation.

LEGEND: AHC= anterior horn cell; CT, cortical; FT, reticular tegmental nuclei; LC, locus ceruleus; P, peribrachial region; PT cells, pyramidal cells; RN, raphe raphe nucleus; nucleus; TC, thalamoc thalamocortic ortical; al; III, oculom oculomoto otorr nucle nucleus us;; IV, troch trochlea learr nucleu nucleus; s; VI, trigeminal motor nucleus. The network of neurons responsible for generating REM sleep is distributed over many levels of the brain. The network is shown as three three system systems s of neuro neurons ns that that mediat mediate e the electrographic phenomena of REM sleep (see Figure above). •

NEURAL NEURAL SUBSTRA SUBSTRATES TES & CREATION CREATION OF SLOW-WAVE SLEEP (NREM SLEEP)

In many places (the thalamus and cortex), the architecture of the systems is known to be far more complex than indicated here. An increase in the firing of reticular, thalamocorticular, and cortical neurons DESYNCHRONIZED

the EEG (fast, irregular waves of REM sleep similar to wakefulness). wakefulness). •









Tonic Tonic disinh dis inhibi ibitio tion n and phasi phasic c excitation of burst cells results in pontine-g pontine-genic eniculate ulate-occ -occipita ipitall (PGO) waves. Phasic Phasic firing firing by reticu reticular lar and vestibular cells causes RAPID EYE movements; vestibular (vestibular nuclei) cells directly excite oculomotor oculomotor neurons.



Tonic postsynaptic inhibition of spinal ante anteri rior or horn horn cell cells s by the the pontomedullary reticular formation causes MUSCLE ATONIA.

Muscle twitches occur occur when excitation by reticular and “pyramidal tract” tract” motor motor neurons neurons (cortico (corticospin spinal) al) occasionally overcomes the inhibition of the anterior horn cells.

NEUROCH NEUROCHEMIS EMISTRY TRY OF SLEEP SLEEP AND WAKEFULNESS (NEUROTRANSMITTERS & SLEEP FACTORS)

Legend Legend and Explanati Explanations: ons: LC – Locus ceruleus (noradrenergic neurons); DRN – Dorsal Dorsal Raphe Raphe nuclei nuclei (seroton (serotoninerg inergic ic neuron neurons) s).. LC and DRN neuron neurons s are are in the brai brains nste tem m reti reticu cula larr form format atio ion) n).. Ch 1- 4 – cholinergic neurons in the forebrain; CH 5 – choliner cholinergic gic neurons neurons in the midbrain midbrain tegmentum.

State-dependent changes in aminergic and cholinergic neuronal function. Sche Schem matic atic repr repres esen enta tati tion on of  progressive decrease of aminergic neurotransmitter release in cerebral cortex as an animal passes from wakefulness through NREM to REM sleep. Cor Cortic tical conc oncentr entra atio tions of  norepinephrine and serotonin are highest in waking, lowest in REM sleep, and intermedi intermediate ate in NREM sleep. Top panel illustrates sagittal sections of the brain with aminergic neurons of nucleus locus coeruleus (noradrenergic) and dorsal raphe nucleus (serotonergic).

Bottom panel illustrates cholinergic neurons of Ch 1-4 (in basal forebrain) and of Ch 5 of  peribrac peribrachial hial pontine pontine tegmentum tegmentum.. Choliner Cholinergic gic neurons release levels of acetylcholine as high in REM sleep as they are in waking; release in NREM sleep is lower.

The graph below summarizes the changes in levels of activity of  serotonin serotoninergi ergic, c, noradrene noradrenergic rgic and cholinergic neurotransmitter systems



Decreasing noradrenergic, cholinergic pontine and serotoninergic activity

tegmentum characterizes drowsiness and NREM (slow-wave) sleep. •



There is almost silent activity of these serotoni serotoninergi nergic c and noradren noradrenergic ergic systems in REM sleep, while the cholinergic system increases its activity again (cholinergic neurons in the pontine reticular formation).





Wakefulness is characterized by high levels of noradrenergic, noradrenergic, serotoninergic and choliner cholinergic gic activity, activity, (Note (Note similarity of increased cholinergic activity in REM with that of  wakefulness.)

[Note that in current sleep literature, seroto serotonin nin’s ’s role role is dis disput puted, ed, as there there was this old serotonin hypothesis about sleep. However, sleep researchers have confirmed the discussion above with evidence for sero seroto toni nin’ n’s s role role (an (an incr increa ease se in concentration) in wakefulness, and not serotonin sleep, sleep, thus thus debunk debunking ing the the old serotonin hypothesis.]

OTHER SLEEP-INDUCING FACTORS: Muramyl peptides (related to the bacterial cell walls) Interleukin – 1 ( a cytokine that may mediate effects of muramyl peptides, and immune responses) Adenosine Delta-slee Delta-sleep p inducing inducing peptide peptide (a substance isolated from blood of  sleeping rabbits) Prostaglandin D2 – Cis-9,10-octadecenoamide Cis-9,10-octadecenoamide MELATONIN – mixed results Othe Otherr sleep sleep pept peptid ides es – the the sear search ch continues

o



• •

• • •

SOME SLEEP DISORDERS

Problems associated with NREM (slow-wave) sleep: o Sleepwalking (somnambulism) - Slee Sleepw pwal alke kers rs aris arise e from from the the slow slow wave wave slee sleep p stag stage e in a state of low consciousness and perform activities that are usually performed during a state of full consciousness. o





Insomnia - Sub Subjec jective tive pro problem blem of  insuffici insufficient ent or nonresto nonrestorati rative ve sleep despite an adequate opportunity for sleep



BedBed-we wett ttin ing g (noc (noctu turn rnal  al  enuresis) - Invo Involu lunt ntar ary y urination while asl eep afte afterr the the age age at which hich bladder contro controll usuall usually y occurs. Night terrors - pavor nocturnus, nocturnus , - Chara Characte cteriz rized ed by extrem extreme e terror terror and and a tempor temporary ary inabil inability ity to regain regain full full consciousness. - Subj Subjec ectt wakes wakes abru abrupt ptly ly from from slow wave sleep with waking usuall usually y accom accompan panied ied by gasp gaspin ing, g, moan moanin ing, g, or screaming while waking. It is often impossible to awaken the person fully because they are so concen concentra trated ted on waking, and after the episode the subje subject ct norma normally lly settl settles es back to sleep without waking. A nigh nightt terr terror or can can rare rarely ly be recalled by the subject. They typically occur during NREM.

Problem associated associated with REM (paradoxical) sleep: o Narcolepsy  - Diseas Disease e in which which there there is episodic episodic sudden loss of 

-

o

o

musc muscle le tone tone and and an eventually irresistible urge to sleep during daytime activities Symp Sympto toms ms:: o Cataplexy Atonia which occurs when one is wide awake. o Unknown cause but may be due to orexin receptor defect or orex orexin in synt synthe hesi sis s dysfunction. o Orexins (hypocretins) (hypocretins) are hypoth hypothala alami mic c peptides. o An auto auto-i -imm mmun une e hypoth hypothesi esis s exists exists,, which results in brain orexin deficiency.

Sleep apnea - Caused Caused by obstruc obstruction tion of the airway during inspiration - Freque Frequent nt in obes obese e and and elderly patients - Cause Cause tirednes tiredness s and poor poor performance due to lack of  sleep - Lack Lack of muscle muscle tone tone of  genioglossus muscle REM behavior disorder  - Newly Newly recog recogniz nized ed condi conditio tion n in which which hypoto hypotonia nia fails fails to occur during REM sleep - They “act out their dreams” dreams”

VII. CLINICAL USES OF EEG •







Helps Helps in locali localizin zing g pathol pathologi ogic c processes Aids in diagnosing and localizing cond condit itio ions ns such such as subd subdur ural al hematomas. Lesions in cortex may cause local formation of irregular or slow waves. Epilepsy o Syndrome with multiple causes o Seizures are divided into:



Partial/ local seizures Arise from only one hemisphere General-onset seizures Invo Involv lves es both both hemisphere Further subdivided into: •







General-onset seizures are further divided into: (1) Grand mal type Loss of consciousness Occurs without warning Follow Followed ed by a tonic tonic phase phase (sust (sustain ained ed limb muscle contraction; fast EEG activity)Followed by a clonic phase (symmetric jerking of limbs; slow waves) • • •

(2) Petit mal Momentary loss of responsiveness responsiveness •

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