Sleep

Slides available at:

www.ucl.ac.uk/lapt/med

Tony Gardner-Medwin,

Physiology room 331

ucgbarg@ucl.ac.uk

Clinical Problems Characteristics Changes in CNS Deprivation Control

Good textbook: Kandel & Schwartz – Principles of Neural Science

[ But they nearly all are adequate ]

SUMMARY

1. Sleep is not 1 state, but 2 radically different states

2. The brain is not resting, but is active (in altered ways)

3. The brain is (arguably) conscious, but very poor at remembering what it was experiencing.

Three conclusions :

INSOMNIA& poor sleep

Problems withwaking tasks

Psychological/Psychiatricproblems

Sleep apnoea

Shiftwork, jetlag

NARCOLEPSY(sudden daytime sleepiness) &CATAPLEXY(sudden paralysis)

HYPERSOMNIA(night & day)

Principal Clinical Problems associated with sleep

Risk of DeathSleep asthma

?? Some cot deaths?

??

• Electroencephalogram (EEG)• Invasive recording of ‘field potentials’ summed from many cells• Single cell recording in

unanaesthetised animals (extracellular)

• Lesions• Stimulation• Pharmacological intervention• Psychophysics (sensory performance)• PET, MRI yet to have much impact

CC

EOG

Frontal

Parietal

Occipital

EEG

Techniques for studying the sleeping brain

SWS

Slow Wave Sleep REM/Paradoxical Sleep

EEG Large Amplitude Low Amplitude (cf waking)

Slow Waves ~ 1 Hz (but theta rhythm in hippocampus)

MUSCLES Reduced tone Total relaxation (e.g. in postural & neck muscles)

SPINAL Some reduction Strong descending inhibitionREFLEXES of motoneurons

AROUSAL to ‘significant’ stimuli Raised threshold (deep sleep)but often waking from REM

PHASIC Muscle twitches Sudden eye movements (REM)EVENTS Sudden CNS discharges

REPORTS ‘dreams’ 0-50% ‘dreams’ 80%-90% ON WAKING & ‘thinking’

Slow Wave Sleep REM/Paradoxical Sleep……ctd….

REPORTS ‘dreams’ 0-50% ‘dreams’ 80%-90% ON WAKING & ‘thinking’

- but NB poor recall unless immediately after rapid arousal

% of SLEEP 60% - 85% ~40% infants~20% most of life~15% old age

WHEN Initially and in cycles Not initially (except narcoleptics)~ 90 min cycle

1. Altered neuronal firing patterns & increased synchrony

Changes in CNS Activity

AWAKE

SWS

REM

Single pyramidal tract neuron activity in monkey motor cortex

1. Altered neuronal firing patterns & increased synchrony

2. Cutting off sensory inflow, e.g. at LGN

Changes in CNS Activity

SWS

Awake

Awake

Responses from cat LGN (lateral geniculate nucleus) to 0.1 Hz visual stimulation. Brainstem sectioned.

1. Altered neuronal firing patterns & increased synchrony

2. Cutting off sensory inflow, e.g. at LGN

3. Cutting off motor outflow by descending inhibition (NB brainstem lesions and 5HT (serotonin) depleters can prevent this)

4. Different “connectivity” of brain, e.g. “PGO” waves (Pons – Geniculate – Occiptal cortex)

- visual cortex gets signals from the brainstem instead of from the eyes during REM sleep

Changes in CNS Activity

Activity in cat optic radiation (LGN projection to visual cortex).Awake and in paradoxical (REM) sleep

Visual cortex

Optic chiasma

Optic radiation

LGN

1. Decreased sleep latency2. Microsleep episodes (& can be EEG slow waves)3. Poor performance in long boring tasks (?=2) but short term

performance usually normal4. Irritability, bizarre statements, paranoia (? ~ cf. schizophrenia)5. Increased % of SWS on recovery night (though only <~30% of

lost sleep is recovered)6. In animals can -> death after ~ 2 weeks, associated with

metabolic and immune abnormalities.

Effects of Total Sleep Deprivation

Effects of REM Deprivation• 1 - 4 above, similar to total sleep deprivation• Becomes difficult to arouse or shift from REM• (5) is opposite: Increased REM on recovery night, and

decreased latency to REM• Possible improvement of affect in endogenous depression and

bipolar disorder

Nuclei of certain known chemicalneuro-modulatory systems• AcetylCholine: Tegmentum [PGO]• Noradrenaline: Locus Coeruleus [Arousal]• 5HT (serotonin): Raphe [Arousal, SWS]

Arousal and Neuro-modulatory Systems

Thalamus

Diffuse projection from RETICULAR ACTIVATING SYSTEM (R.A.S.) -> arousal

‘Specific’ sensory signals to thalamus and cortex

‘Non-specific’ collaterals of sensory axons go to RETICULAR ACTIVATING SYSTEM (R.A.S.)

Sleep

www.ucl.ac.uk/lapt/med Please use the Web Discussion Forum for problems/queries

Tony Gardner-Medwin,

Physiology room 331

ucgbarg@ucl.ac.uk