Sleep wake cycle and insomnia

-when awake, areas in the brainstem and hypothalamus called arousal centres stimulate the cerbral cortex -arousal centres release neurotransmitters including ACh, histamine,5HT and orexin

-the ventrolateral preoptic nucleus in hypothalamus switches off arousal centres -VPLO produces neurotransmitters GABA and galanin -neurotransmitters cause arousal centres to shut down resulting in rapid changes into NREM sleep

-mutual inhibition between wake-promoting neurons from the arousal centre and sleep-promoting neurons from the VPLO -when cortex is activated by the sleep arousal centres there is a simultaneous inhibition of VLPO

histamine,5HT,NA stimulate the cortex promoting wakefullness and stops the messsage that makes us sleep

-if histamine is released and inhibited then sleep will ensue -happens because the VPLO blocks the production of histamine and other wake signs by GABA and galanin -but histamine also blocks VPLO in which case switch will flip to wake state

awake-GABA and galanin sleep - histamines

-24 hour circadian rythum of sleep and arousal-proccess c -a sleep wake timer-homeostatic mechanism-proccess s

-the suprachiasmatic nucleus communicates the circadian rhythm to the body via the production of melatonin -melatonin production by the pineal gland peaks in the middle of the night. -melatonin does not induce sleep but simply signals the start of sleeping process

Tendency to sleep​ Sleep structure​ Level of alertness​ Temperature regulation​ Hormone production​ Melatonin​ Growth hormone​ Cortisol​ Cardiovascular function​ Respiratory function​ Glucose levels

every daytime by light and every night time by melatonin

-Homeostatic mechanism ‘counts’ how long we have been awake or asleep and a ‘sleep pressure’ builds up with increasing wakefulness​ -The longer you remain awake, the higher the sleep pressure​ -As you sleep, the sleep pressure reduces and the likelihood of awakening increases

the accumulation of adenosine in the cerebrospinal fluid whilst awake

-Adenosine is released from ATP as energy from glycogen is used during the day so levels increase the longer you are awake​ -Adenosine levels will drop during sleep as glycogen stores are replenished​ -Stimulants such as caffeine and theophylline (tea and chocolate) act as adenosine receptor antagonists and so reduce its ability to induce sleepiness

-during the first half of sleep the sleep pressure is still high whilst the circadian alerting signal has decreased -sleep drive now has been reduced however the persistant low circadian alerting signal maintains sleep -synchronization of these two systems allow consolidation periods of both alertness and sleep

-light -pain -medical condtions -medication -alcohol -caffeine -sleep environment

-light modulates circadian rhythm by influencing the timing of SCN -light stimulates photosensitive cells of the retina which signal to the SCN via retinohypothalamic tract -exposure to light during the night can reset the internal clock making sleep diffcult

-alpha and beta blocker reduce REM and NREM3 sleep and increases daytime sleepiness -some antideppresants provoke insomnia, reduce REM sleep -brain cells promoting alertness are inhibted by adenosine

it is an adenosine receptor antagonist and so removes the inhibition by adenosine resulting in increased alertness

-insomnia -sleep related breathing disorders (obstructive sleep apnoea -central disorders of hypersomnolence-narcolepsy -circadian rhythm sleep wake disorders -parasomnias -sleep related movement disorders

-chronic insomnia disorder -short term insomnia disorder -other insomnia disorder -isolated symptoms and normal variant

-difficulty initiating sleep -difficulty maintaining sleep -waking up earlier than desired

At least three times a week -has been present for at least 3 months

p-main condtion s-caused from another condition

-Psychophysiological insomnia -idiopathic insomnia -paradoxical insomnia