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have when awake but relaxed,drowsy, often with eyes closed, not aroused or excited.
regular meduim frequency waves of 8-12 Hz |
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when awake and alert, attentive, thinking
irregular mostly low amptitude waves of 13-30 Hz
shows DESYNCHRONY-reflects that many different neural circits are activated |
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| during early stages of slow wave sleep and REM sleep, EEG activity of 3.5-7.5 Hz |
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| occurs during deepest stages of slow wave sleep, regular, synchronized EEG activtiy during its deepest stages |
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| Stage 1-transitions between alpha and beta, transition beween sleep and wakefulness, about 10 mins stage 2-theta activity, sleep spindles (short bursts of waves of 12-14 Hz that occur 2-5x a minutes during stages 1-4) and K complexes (sudden sharp waveforms, usually found only during stage 2). At this point person is sleepin soundly, but if awakened mught deny they were asleep. About 15 mins Stage 3 and stage 4-called slow wave sleep, High amplitude delta activity, more delta activity in stage 4, deepest stage of sleep, may act groggy and confused if wakened REM sleep-after 90 mins from falling asleep, rapid eye movement, paralyzed, dreaming during this stage, wakes easily to meaningful stimuli and may appear alert and attentive when woken up,increased cerebral metabolism and veginal secretions and erections, lasts 20-30 mins Rest of night, goes through cycles of REM and nonREM, each cycle about 90 mins long and contains 20-30 mins of REM, slow wave sleep occurs mostly during first half of night |
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| affects 25% occasionally and 9% regularly. No objective definition, usually based on people subjective reports, most people are treated by GP with meds, people underestimate amount of sleep they get |
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| cessation of breathing while sleeping.Usually caused by airway obstruction that can be relieved surgically or treated with mask providing pressurized air, common in obesity, causes cognitive deficits if not treated |
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“rare” neurological disorder (1 in 2,000. Onset usually by 15-30; 6% <10 years old. Characterized by sleep attacks, with almost instantaneous onset of REM sleep for 2-3 mins usually during boring conditions. May skip slow wave sleep at night, or fall instantly into REM sleep from wakefulness. Sleep is fragmented
caused by a heriditary autoimmune disorder in which during adolescence the immune system attacks the nuerons which produce orexin (a peditde which excites brain nuclei with important roles in wakefulness.
Stimulants can treat sleep attacks, antidepressants can treat cateplexy |
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| feature of narcolepsy-momentary paralysis of muscle weakness without loss of consiousness occuring in association witsudden emotional reactions of physical discomfort |
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| occasioanl episodes the person can't move, occuring just before or after sleep |
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| hypnogogic hallucinations |
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| vivid auditory or visual hallucinations-dreaming while awake, usually right before or after sleep |
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| REM Sleep Behavior Disorder |
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| Fail to paralyze during REM sleep so often act out dreams. Common is nuerodegenerative disorders like PD, dementia withLewy bodies. Clonazepan is very effective for treatment. |
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| Slow Wave Sleep disorders |
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| bedwetting, somnambulism (sleepwalking), nighr terrors, sleep related eating disorders (2/3rd women, average age 27, most overweight and prefer high caloric food) |
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| possible answers are adaptive response to having frontal lobe (only earn blooded vertebrates have REM sleep), or restorative process, may allow bran to develop, rest and learn (studies show physical activity not affected by sleep loss but cognitive activity is). we dont make up sleep we miss in hours, but REM and stage 4 sleepincrease % wise. Keep animals wout sleep and eventualdeath |
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| results in damage to portions of thalamus, deficits in attention and memory, followed by dreamlike confused state, loss of conrol of autonomic nervous system and endocrine system, and insomnia. Eventully die. |
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may play a role in development of brain-70% of sleep in newborns in REM vrs 30% at 6 months,
may facilite learning-more REM after learning, impaired performnce after learning if sleep deprived.nonecrlarative memory consolidation needs REM and declarative memory consolidation may need slow wave sleep |
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| a neuromodulator that is released by neurons engaging in high levels of metabolic activity, may play a primary role in initiation of sleep. Accumulation of adenosne serves as sleep poromoting sustance, more adenosine acculmulates as wakefulness is prolonged. Increased adenosine causes cognitive/emotional effects of sleep depriation. caffeine blocks adenosine receptors. |
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| five nuerotransmitters that contribute to arousal |
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| Acetylcholine, noreepinephrine, seretonin, histamine, orexin |
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| acetylcoline in dorsal pons and basal forebrain produce activation and cortical desynchrony when stimulated |
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| Norepinephrine neurons in locus coerulus in pons hve widely distributed axons in neocortex, hippocampu, thalamus, cerebellum and medulle, increase arousal |
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| seritonin neurons in raphe nuclei in brainstem project widely to brain, and simulation of raphe nucleu causes locomoion and cortical arousal. |
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| histaminergic neuron cell bodies located in tuberomammilary nucleus of hypothalamus and project to cortex, thalamu, BG, basal forebrain and hypothalamus. directly or indirectly increase cortical activation. antihistamines cause drowsiness. |
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| cell bodies that secrete orexin in hypothalamus, project to most regions of brain, has an excitatory effect by stimulating areasimportant for wakefulness, role in stabuilizing wakefulness and sleep, in narcolepsy orxin neurons attacked by immune system. |
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| Ventrolateral Preoptic Area (vlPOA) |
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| In anterior hypothalamus. A group of neurons in this area screte GABA to supresses alertness and behavioral arousal and promotes sleep. Has a flip flop circut (reciprocal inhiition) so its impossible for both sets to be active at same time. Either viPOA is active and arousal systems in basal forebrain and pontine regions are inhibited and person is asleep, or viPOA is inhibited and arousal system is active and person is awake |
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Flip flop mechanism also seen in REM sleep. Sublaterodorsal nucleus-a region of the dorsal pons just ventral to locus coeruleus that forms the REM-ON portion of the REM sleep sleep flip flop. Ventroateral pariaqueductal gray matter-a region of the dorsal midbrain that forms the REM OFF protion ofthe REM sleep flip flop.During waking, the REM-OFF region receives excitatory input from the orexinergic neurons of the lateral hypothalamus, and this activation tips the REM flip-flop into the OFF state. Additional excitatory input from noradrenergic neurons and serotonergic neurons.
When slow-wave sleep begins: Activity of the excitatory orexinergic, noradrenergic, and serotonergic inputs to the REM-OFF region begins to decrease. As a consequence, the excitatory input to the REM-OFF region is removed
The REM flip-flop tips to the ON state, and REM sleep begins. Presumably, an internal clock—perhaps located in the pons—controls the alternating periods of REM sleep and slow-wave sleep that follow |
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| a daily, rythmical change in behavior or physicological process. Some of these rhythms are passive responsises to changes in illumination and other rhythms are controlled by mechanisms within the organism,by internal clocks. |
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| a stimulus (usually the light of dawn) that resets the biological clock that is responsible for circadian rhythms |
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| a nucleus situated atop the optic chiasm that contains a biological clock that is responsible for organizing many of the body's circadim rhythms. Retina has direct projections to the SCN. Melanopsin is a photopigment resent in ganglion cells in retina whose axons transmit info to SCN. SCN controls cycles by direct neural connections and the secretions of chemicals that affect the activity of neurons in other regions of brain. |
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| gland attached to the dorsal tectum,produces melatonin and plays a role in circadian and seasonal rhythms, may be useful to combat jet lag or shifts in work schedule |
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| a hormone secreated during the day by the pineal body, plays a role in circadian and seasonal rhythms |
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