5.4 sleep Flashcards
What is shown on the EEG, EOG and EMG in the awake stage?
- EEG: fairly fast rhythm (beta)
- EOG: Certain amount of eye movement
- EMG: Reasonable level of muscle tone
What is shown on the EEG, EOG and EMG in stages 1& 2 of slow wave sleep?
- EEG: rhythm becomes lower in frequency (alpha)
- EOG: far fewer eye movements
- EMG: reduced muscle tone (more relaxed)
What is shown on the EEG, EOG and EMG in stages 3 &4 of slow wave sleep?
- EEG: rhythm becomes even slower (theta to delta rhythm)
- EOG: minimal eye movements
- EMG: even more reduced muscle tone (more relaxed)
What is shown on the EEG, EOG and EMG in stage 5 REM sleep?
- EEG: Activity becomes much faster (more towards a beta rhythm –> similar to awake)
- EOG: wide discursive movement of the eyes (more than stages 1-4 and awake)
- EMG: even further reduced muscle tone (very relaxed)
The level of arousal is maintained by the reticular activating system (RAS), which consists of a pathway starting in the brainstem:
• ____________________ modulate the activity of the cerebral cortex (either directly or by relaying through thalamic nuclei for the cholinergic nuclei)
• ______________ also projects to the cerebral cortex and contributes to its modulation
• These pathways are active all the time (level of activity varies) → the higher the level of activity, the more activated the cortex is, and the more alert the patient feels
cholinergic nuclei, raphe nucleus, nucleus coeruleus;
Hypothalamic nucleus (tuberomammillary nucleus);
what is the function of the ventroateral preoptic nucleus (VLP) in controlling the passage from sleep into wakefulness and vice versa
Tends to inhibit the RAS by inhibiting the activity of the contributing nuclei (both in the brainstem & hypothalamus) → induction of sleepy state
what is the function of the lateral hypothalamic nuclei (LH) in controlling the passage from sleep into wakefulness and vice versa?
Tends to excite the activity of the contributing nuclei, which increase the activity passing through the RAS → increases the level of arousal
The __________________ controls REM (stage 5) sleep, specifically in pushing an individual into REM sleep:
• Able to suppress muscle tone and sensory input
• Activates eye movements through connections to the cranial nerve nuclei in the midbrain (particularly CN ____________________)
caudal pontine reticular formation (CPRF);
III, IV, VI
The circadian synchronisation of the sleep-wake cycle (to the day-night cycle) occurs via the ___________________ found in the hypothalamus:
• Lies just superior to the _______________ (carries information from retina via optic nerve)
• Special ganglion cells within the retina do not participate in the usual visual process of producing images → respond to the presence of light instead
o SCN becomes activated as daylight decreases, resulting in many projections to the nuclei involved in controlling the level of arousal or the sleep-wake cycle → pushes the individual towards a state of drowsiness
• Possesses projections to the _______________ (lies in the root of the 3rd ventricle towards the back) → secretes melatonin
o SCN becomes activated at the end of the day as daylight decreases, and the shift of the sleep-wake cycle towards sleep results in melatonin release
o Melatonin causes widespread effects on other bodily functions (e.g. adjustments in energy levels, blood pressure, various hormone levels)
suprachiasmatic nucleus (SCN); ;
optic chiasm
pineal gland;
what are chronic causes of insomnia?
Physiological (sleep apnoea, chronic pain) Brain dysfunction (depression, FFI)
- Fatal familial insomnia (FFI) is a rare prion disease causing a lesion of the brainstem → progression of lesion causes sleep loss → eventual death
what is the cause of narcolepsy (falling asleep without warning)
- Associated with cataplexy (sudden reduction in all muscle tone)
- Likely due to dysfunction of control of REM sleep caused by orexin deficiency
what are treatments for insomnia?
most hypnotics (enhance GABAergic circuits), behavioural techniques (taught to relax and improve sleep)
what are treatments for narcolepsy?
stimulants (e.g. amphetamines), some attempts to restore orexin (mixed success in clinical trials)