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Dr. Keith Hearne's PhD Thesis

LUCID DREAMS:

An Electro-Physiological and Psychological Study

First PhD in the world on the topic of lucid dreams

First eye-movement signalling from within the lucid dream state

Discovery of the pre-lucid REM burst

Discovery of basic physiological parameters of lucid dreaming

(c) Copyright Dr Keith Hearne, 1998. All rights reserved.

Copyright exemption :

Copies of those original chart records may be down-loaded HERE and may be reproduced in publications by others providing the appropriate source is added :

Hearne, K. (1978) Lucid dreams - an electro-physiological and psychological study. PhD thesis. Dept. of Psychology, University of Liverpool, England (May 1978).  (Available at : www.european-college.co.uk)

N.B.

Dr Hearne's original chart records of signals from within lucid dreams, and his dream machine invention, are now on display at the Science Museum in London.

N.B.

Background to the first PhD in the World on Lucid Dreaming and the original discovery of the ocular-signalling technique from lucid dreams

After obtaining a BSc in psychology from Reading University, England, in 1973, Keith Hearne went to Hull University in the Autumn of that year, intending to conduct research for a PhD on hypnotic dreams, following discoveries he had made in 'hypno-oneirography'. He decided instead to use newly acquired computer equipment to research electro-physiological aspects of visual imagery*. During that time he became skilled in running a sleep laboratory. He became interested in  'lucid' dreaming (the paradoxical conscious awareness of dreaming within the dream itself) and reasoned that it must be possible for a lucid dreamer to communicate to the world of wakefulness. A problem, though, was the inherent muscular paralysis of REM sleep. In 1975 it suddenly occurred to Hearne that since the eye musculature is not inhibited in REM sleep, it might be possible to get subjects to signal by making deliberate ocular movements. On the morning of 5th April 1975, wired up a lucid dream subject who was instructed to make a sequence of left-right eye-movements on becoming lucid. A lucid dream was reported at about 8 am, but unfortunately, the monitoring equipment had just been switched off. A week later, on the morning of 12th April 1975, the same subject had another lucid dream. The first signals in the world from a lucid dream were thus recorded. Hearne continued to obtain more records over the next months. He wound up the work on visual imagery, submitting it for an MSc and moved to Liverpool University, where he was offered a sleep-laboratory, to research lucid dreams for this PhD, using paid subjects. During the course of this work he discovered the basic electro-physiological features of lucid dreams, including the pre-lucid REM burst. He also invented the first 'dream machine'. Subsequently Hearne also discovered the 'light switch' phenomenon.

In 1975 Hearne informed psychology departments at American universities of his findings including Stanford (W. Dement) and Chicago (A. Rechtschaffen).

*Hearne, Keith M.T. (1975) Visually evoked responses and visual imagery. MSc thesis. University of Hull, England.

N.B. A book written by Dr Hearne fully described his research into lucid dreams : Hearne, K. (1990) The dream machine. Aquarian Press, Wellingborough, England.

Other books :
Hearne, K. (1989) Visions of the future. Aquarian Press, Wellingborough, England.

Melbourne, D. & Hearne, K. (1997) Dream interpretation - the secret. Blandford Press, London.

Melbourne, D. & Hearne, K. (1998) The Dream Oracle. New Holland Publishers.

Melbourne, D. & Hearne, K. (1999) The Meaning of Your Dreams. Blandford Press

Hearne, K. & Melbourne, D. (2001) Understanding dreams. New Holland Press.
(Several other books are pending publication).


START OF THESIS

LUCID DREAMS :
An Electro-Physiological and Psychological Study
PhD thesis by Dr Keith Hearne (BSc MSc PhD)

THESIS SUBMITTED IN ACCORDANCE WITH THE REQUIREMENTS OF THE UNIVERSITY OF LIVERPOOL, ENGLAND FOR THE DEGREE OF DOCTOR IN PHILOSOPHY

By
KEITH MELVYN TREVOR HEARNE BSc MSc

- May 1978 -

BSc  University of Reading  1970-73
MSc  University of Hull  1973-75
PhD  University of Liverpool   1975-78

CONTENTS

PhD page number

ACKNOWLEDGEMENTS

ABSTRACT

CHAPTER I. AN OVERVIEW

I.1 AIMS OF THIS RESEARCH  

2

I.2 THE FORMAT       

3

PART 1. INTRODUCTION

CHAPTER II. THE ELECTRO-PHYSIOLOGY OF SLEEP

II.1 BRIEF HISTORICAL BACKGROUND TO ELECTRO PHYSIOLOGY 

7

II.2 ELECTRO-PHYSIOLOGICAL MEASUREMENT

a. Technical points  

10

b. The EEG, EOG and EMG

14

II.3 HUMAN SLEEP-STAGES AND SCORING CRITERIA

CHAPTER III. GENERAL SLEEP-RESEARCH FINDINGS

III.1 THE PHYSIOLOGY OF SLEEP  

23

III.2 THE CHANGING CONCEPT OF SLEEP  

26

III.3 DEVELOPMENTAL ASPECTS OF SLEEP     

29

III.4 THE PHARMACOLOGY OF SLEEP 

31

III.5 SLEEP DEPRIVATION        

33

III.6 MEMORY AND SLEEP  

35

III.7 EXTERNAL STIMULI AND SLEEP     

36

III.8 SIGNALLING FROM SLEEP        

37

III.9 BORDERLAND PHENOMENA  

41

III.10 ABNORMALITIES OF SLEEP 

44

III.11 SLEEP THEORIES 

48

CHAPTER IV. DREAMS

IV.1 ANCIENT INTEREST IN DREAMS   

53

IV.2 EARLY CHRISTIAN VIEWS             

58

IV.3 RELIGIO-POLITICO-CULTURAL DREAMS

59

IV.4 PRE-FREUDIAN DREAM NOTIONS   

62

IV.5 FREUDIAN DREAM THEORY 

68

IV.6 JUNGIAN DREAM THEORY 

79

IV.7 RECENT IDEAS ON DREAMS

83

IV.8 CREATIVITY AND DREAMS 

93

CHAPTER V. LUCID DREAMS

V.1 THE PHENOMENON

96

V.2 THE POTENTIAL IMPORTANCE OF LUCID DREAMS  

98

V.3 CHARACTERISTICS OF LUCID DREAMS

1. The transitional stage   

100

2. The onset of lucidity   

100

3. Lucidity starting from a waking state

102

4. Flying and lucid dreams  

102

5. Physical realism in lucid dreams   

104

6. Psychological realism in lucid-dreams

104

7. Perceptual texture in lucid dreams

105

8. Memory of lucid dreams

107

9. Memory in lucid dreams

107

10. Analytical thought in lucid-dreams   

108

11. Emotional quality of lucid-dreams    

109

12. Controllability of lucid-dreams

111

13. Extra-sensory perception and lucid dreams

112

14. False-awakenings 

113

15. Lucid dreams in 'hypnosis' 

115

16. False lucidity   

117

V.4 WRITERS ON LUCID DREAMS

118

V.5 LUCID-DREAMS IN RELATION TO DREAM THEORIES

124

V.6 EXPERIMENTAL CONSIDERATIONS   

125

 A NOTE ON DEMAND CHARACTERISTICS     

127

CHAPTER VI. PHILOSOPHICAL ASPECTS OF DREAMS 

129

PART 2. THE EXPERIMENTS

CHAPTER VII. THE NEW TECHNIQUE

OVERVIEW

135

VII.1 INTRODUCTION   

138

VII.2 METHOD    

139

VII.3 RESULTS

144

VII.4 CONCLUSIONS  

145

CHAPTER VIII. THE 1st A.W. STUDY - ELECTROPHYSIOLOGICAL FINDINGS

VIII.1 INTRODUCTION

147

VIII.2 METHOD 

148

VIII.3 RESULTS    

151

VIII.4 DISCUSSION    

157

VIII.5 CONCLUSIONS 

161

CHAPTER IX. THE 1st AW STUDY - PSYCHOLOGICAL FINDINGS

IX.1 INTRODUCTION

184

IX.2 RESULTS      

186

IX.3 DISCUSSION   

206

IX.4 CONCLUSIONS

207

CHAPTER X. OTHER LUCID-DREAM SUBJECTS

X.1 INTRODUCTION 

210

X.2 METHOD  

210

X.3 RESULTS    

211

X.4 DISCUSSION   

216

X.5 CONCLUSIONS   

217

CHAPTER XI. SIMULATING CONTROL EXPERIMENT

XI.1 INTRODUCTION 

219

XI.2 METHOD  

220

XI.3 RESULTS  

221

XI.4 DISCUSSION   

224

CHAPTER XII. LUCID-DREAM INDUCTION EXPERIMENT

XII.1 INTRODUCTION

226

XII.2 METHOD

227

XII.3 RESULTS     

228

XII.4 DISCUSSION      

230

XII.5 CONCLUSIONS   

231

CHAPTER XIII. THE 2nd AW STUDY

XIII. 1 INTRODUCTION      

235

XIII.2 METHOD 

237

XIII.3 RESULTS    

239

XIII.4 DISCUSSION

242

XIII.5 CONCLUSIONS

244

CHAPTER XIV. ADDITIONAL DATA FROM SUBJECT A.W.

XIV.1.FREQUENCY DATA

XIV.1.1 INTRODUCTION

253

XIV.1.2 RESULTS  

253

XIV.1.3 DISCUSSION    

255

XIV.2 DIARY DATA

XIV.2.1 INTRODUCTION 

256

XIV.2.2 METHOD 

256

XIV.2.3 RESULTS  

257

XIV.2.4 DISCUSSION 

258

XIV.3 POST-LUCID-DREAM QUESTIONNAIRE DATA

XIV.3.1 INTRODUCTION

260

XIV.3.2 METHOD 

260

XIV.3.3 RESULTS    

260

XIV.3.4 DISCUSSION   

267

XIV.4 OVERALL CONCLUSIONS     

268

CHAPTER XV. QUESTIONNAIRE INFORMATION

XV.1 INTRODUCTION  

271

XV.2 METHOD  

272

XV.3 RESULTS     

273

XV.4 DISCUSSION  

278

XV.5 CONCLUSIONS 

279

CHAPTER XVI. PERSONALITY AND INTELLECTUAL CAPACITY IN RELATION TO LUCID-DREAMS

XVI.1 INTRODUCTION 

285

XVI.2 METHOD      

289

XVI.3 RESULTS  

290

XVI.4 DISCUSSION

291

PART 3. DEVICES

DEVICES : GENERAL INTRODUCTION

CHAPTER XVII. 'CEMOS' DEVICE

293

XVII.1 INTRODUCTION

295

XVII.2 DESCRIPTION OF THE APPARATUS 

296

XVII.3 COMMENTS    

296

CHAPTER XVIII. NIGHTMARE INTERRUPTER DEVICE

XVIII.1 INTRODUCTION    

299

XVIII.2 DESCRIPTION OF THE DEVICE    

305

XVIII.3 PROPOSALS  

306

CHAPTER XIX. LUCID-DREAM / FALSE-AWAKENING
INDUCTION DEVICE

XIX.1 INTRODUCTION

309

XIX.2 DESCRIPTION OF THE DEVICE      

309

PART 4. DISCUSSION AND CONCLUSIONS

CHAPTER XX. DISCUSSION AND SPECULATIONS

XX.1 SURVEY OF THE FINDINGS 

313

XX.2 OTHER POINTS AND SPECULATIONS   

322

CHAPTER XXI. CONCLUSIONS AND SUGGESTIONS FOR FURTHER RESEARCH

XXI. CONCLUSIONS

328

XXI.2 SUGGESTIONS FOR FURTHER RESEARCH 

333

REFERENCES  

337

APPENDIX  

366

 

(END)    

418

 


ACKNOWLEDGEMENTS:

 

I should like to thank Dr Jake Empson (my MSc Supervisor) of Hull University for providing me with a knowledge of sleep-research technique , and my current Supervisor, Dr Graham Wagstaff, for his valuable comments on my work.

I should especially like to thank the main subject in this study, Alan Worsley of Hull, for his great co-operation over the 3 years of experimentation. Also, all the other subjects who volunteered to spend nights in the sleep-laboratory with no remuneration.

The Department’s workshop staff, under Eric Britton, deserve credit for their friendly efficiency in providing equipment, and I am grateful to Brian Mitchell and Eddy Cookson for designing and constructing the 'CEMOS' device to my specifications.

Keith M.T.Hearne

Dept. of Psychology

University of Liverpool. May 1978.

 


 

ABSTRACT :

The aim of this research was to make original investig­ations into ‘lucid-dreams’ (those in which the dreamer has insight that the experience is a dream). A new method of ocular signalling from these dreams was discovered, so circumventing the bodily paralysis of Stage REM sleep, and establishing a mode of communication from the sleeping subject.

All-night Polygraphic recordings were obtained from 18 subjects who reported having lucid-dreams. However, after extensive monitoring only two of the eighteen subjects were able to produce lucid-dreams in the laboratory. Much physiological and psychological information on these dreams in the best subject was made available using the new technique. All the lucid-dreams occurred in Stage REM sleep and had a mean duration of 4 minutes. There were no differences in the sleep-patterns between Control and lucid-dream nights. The temporal order of events reported on waking corresponded in general to the signalled information. A group of simulating Control subjects were unable to reproduce ocular signals with REM EEG on waking from Stage REM sleep. Additional data was analysed concerning home lucid-dreams. A 4-day cycle accounted for 25% of the subject’s lucid-dreams and they tended to occur more after days of above average stimulation.

A large group of persons who reported having lucid-dreams provided questionnaire data. Personality and intelligence factors were also studied in relation to these dreams, but no significant findings resulted.

A method of induction of lucid-dreams was tried unsuccess­fully on a group of subjects, but a later technique showed promise. A study of 2-way communication between subject and experimenter was inconclusive.

Three inventions were devised as a result of this research: a switching device operated by ocular signals; a device for waking persons at the early stage of nightmares ; a device to induce lucid-dreams and false-awakenings.

 


CHAPTER I

I.1 AIMS OF THIS RESEARCH

The purpose of this programme of research was to investigate a remarkable type of dream (the 'lucid' dream) in which, reportedly, consciousness and volitional control are present i.e. the dreamer has insight whilst dreaming that the experience is a dream and can, to some extent, manipulate dream content and course of action. Very little appeared to be known about lucid-dreams, yet it seemed that, potentially, they held the key to unravelling much about dreams generally, and also could assist the understanding of other psychological processes such as memory and thought.

It seemed not unreasonable to suppose that suitable subjects could report information from ongoing lucid-dreams in some way. This would provide knowledge on dreams from within the dream for the first time. Obviously, a signalling technique (from the subject) would first have to be devised, though.

A primary aim of the research programme therefore was to obtain subjects who report having lucid-dreams and perform all-night polygraphic monitoring on them. Providing a signalling method could be established, basic electrophysiological data was to be ascertained about lucid-dreams, together with psycho­logical information. One objective was to determine whether lucid-dreams are in fact true dreams occurring in Stage REM sleep, or whether they are a phenomenon of imagery experienced on waking. Electrophysiological monitoring of subjects could answer that question. Since no previous work appeared to have been conducted on lucid-dreams, the actual course of experimentation in that respect would develop as findings became available.

In addition to polygraphic monitoring of lucid-dream subjects, it was planned to attempt the artificial induction of lucid-dreams in subjects in order to make research more efficient. Also, questionnaire data from lucid-dreamers would be obtained and analysed to seek any connections between various imagery and sleep phenomena, in the hope of finding clues as to any possible causes of lucid-dreams. Another aim would be to develop any devices which might be useful regarding the induction of lucid-dreams or as aids in experimentation.


CHAPTER I

I.2 THE FORMAT

This thesis consists of four main parts. The first is introductory, consisting of information on : The methodology con­cerning the electrophysiological study of sleep and dreams ; general sleep-research findings ; the history of dreams and various dream theories ; collated data on the waking accounts of lucid-dreams ; philosophical aspects of dreams. These areas are covered in five Chapters.

In the second part, the experiments are described in detail. The programme followed the plan outlined in I.1. One of the lucid-dreamers was particularly co-operative and produced much valuable sleep-lab and questionnaire data. Once a method of signalling was perfected, one precautionary study involved seeing whether simulating Controls could reproduce the same type of signal when woken from Stage REM sleep. Another study which later suggested itself on the basis of earlier findings was that of testing personality and intelligence factors of subjects in relation to their reported frequency of experiencing lucid-dreams. In all, 10 Chapters catalogue the experimentation performed in this research.

Part 3 (three Chapters) consists of descriptions of three devices which were developed as a direct result of this research. The first would aid lucid-dream research, but is still in the developmental stage. Another device is designed to wake persons from the early stage of nightmares. The third device is intended to induce lucid-dreams and false-awakenings. Part 4 of this thesis consists of two Chapters in which the experimental results are discussed and various theoretical speculations are proposed, and overall conc­lusions are listed and suggestions for further research are stated.


CHAPTER II

II.1 BRIEF HISTORICAL BACKGROUND TO ELECTRO-PHYSIOLOGY

Galvani (c 1790) discovered that the current generated by two dissimilar metals applied to the crural nerve in the leg of a frog caused twitching of the attached muscle. This demonstration showed that nerves conduct electrical impulses rather than some 'vital fluid' - a view that had held for centuries and was most elaborately propounded by Descartes (Lindsley & Wicke, 1974 ; Sheer, 1961.) Later, Nobili (1827) first measured electrical activity in frog muscles.

When technical developments in current detection permitted, Caton (1875) at Liverpool university performed the first published experiments in monitoring the very small electrical activity from the exposed brains of rabbits and monkeys. Caton observed a constantly changing background current and changes at the sensory surface of the brain during sensory stimulation.

At the beginning of this century, several investigators began to study muscles and nerves electrically, and in the 1920s electronic amplification became available for electro-physiological work following the development of the vacuum tube.

The neuro-psychiatrist Hans Berger (1929) at the university of Jena published an account of the recording of electrical activity from the scalps of human subjects (Gloor, 1969). He reported the discovery of rhythmic 10Kz waves (which he termed 'alpha waves') in subjects with eyes closed. In addition, he observed smaller amplitude faster frequency activity which he called 'beta waves'.

He also termed the whole record the 'Elektrenkephalogram' (EEG). For electrodes, Berger used two large saline pads on the forehead and occiput.

His findings were treated sceptically by other electro-physiologists until Adrian & Matthews (1934) replicated his results. Many varied investigations then began and the rapid advancements in equipment (e.g. multiple channel recording, cathode-ray oscilloscope monitoring) aided this work.

Apart from animal studies, investigations were initiated to seek physiological, psychological and pathological correlates of the EEG in humans. Loomis, Harvey & Hobart (1935, 1936) observed the EEG of sleep and noted vast changes during that state.

Berger's original observation that epilepsy and other neurological disorders produced an abnormal EEG was taken up by others. Dawson (1951) introduced an 'averaging' technique for teasing out minute evoked responses from the background EEG. W.G. Walter, Cooper, Aldridge, McCullum & Winter (1964) first observed a slow negative potential (d.c.) shift associated with anticipation - the Contingent Negative Variation (CNV).

From the point of view of sleep research, a most important discovery was that of the different sleep-stages - including REM (Rapid-Eye-Movement) sleep, which was shown to be associated with subjective reports of dreaming (Aserinsky & Kleitman, 1953) ; Aserinsky & Kleitman, 1955 ; Dement & Kleitman, 1957b).


CHAPTER II

 

II.2 ELECTRO-PHYSIOLOGICAL MEASUREMENT

- a. Technical points

AMPLIFIERS

The minuteness of electro-physiological measures, especially the electro-encephalogram (measured in millionths of a volt), necessitates the use of very sensitive high-gain amplifiers for monitoring and recording purposes. In modern research, multiple-channel high quality instruments (polygraphs), often linked to computers, enable the sophisticated recording and analysis of data. A typical instrument is equipped with variable time-constant, variable chart speed and electronic filtering facilities.

ELECTRODES

The interface between skin and recording instrumentation is of crucial importance in obtaining accurate measurement. High-conductivity silver electrodes coated with silver-chloride are commonly employed in electro-physiological work. Their relative non-polarising characteristic permits direct-current potentials to be recorded without a constant signal shift. Electrodes need to be firmly attached with collodion glue (where hair is present) or surgical tape to the skin.

 

ELECTRODE GEL

Electrolytic past or gel - a chloride salt of a formula consistent with the chemistry of the epidermis, is placed between the electrode and skin, to conduct the electrical potentials. A grease solvent such as acetone is used to cleanse the skin so reducing skin-resistance before attachment of electrodes.

 

ARTEFACTS

A number of sources of artefact exist which can obliterate or modify measured potentials. For instance, skin-stretching occurring when the subject moves, can cause high-voltage transients. Electrical interference ('mains hum') is another potential bug-bear which may be present when electrodes are poorly attached or the subject not grounded.

Bias potential results from two electrodes having an imbalance in ionic transfer, due to different metallic properties or surface contamination.

Polarisation is a back-electromotive force occurring as a result of electrolysis between the electrode and electrolyte - in one direction, so either increasing or decreasing the true potential. (Thompson & Patterson, 1974 ; Greenfield & Sternbach, 1977).


CHAPTER II

- b. The electro-encephalogram (EEG), electro-oculogram (EOG) and electro-myogram (EMG)

The electro-encephalogram is a graph of voltage plotted over time, measured from the most superficial layers of the cerebral cortex (Stevens, 1974). The frequency and amplitude of the monitored brain activity provide the basic data for the encephalographer. Two modes of electrode placement exist i.e. monopolar (referential) or bipolar. In the former case there is an active recording electrode which is 'referred' to an 'indifferent' electrode positioned on a supposedly electrically neutral site such as ear-lobe. In bipolar recording, the signal represents the difference electrically between the two electrodes.

The international 10/20 system of electrode placement (Jasper, 1958) has been widely adopted for EEG recording. This uniform system enables a better comparison of studies from different laboratories. Electrodes are positioned at points on imaginary circles 10 or 20 percent of the distance along the axes from nasion to inion and preauricular points coronally (Figure I.1, page 17). Gibbs & Gibbs (1964) criticised the 10/20 system as being geometric rather than satisfying the requirements for the best electrical placements. Remond & Torres (1964) modified the 10/20 system for use with infants and small children.

In the normal EEG there are four main frequency bands. Changes in the predominance of different bands occur during maturation (Lindsley & Wicke, 1974). These bands are :

 

DELTA

W.G. Walter (1937) introduced this term to describe certain 'high voltage' (perhaps a few hundred microvolts) slow waves of a frequency of 0.5 to 3Hz. Delta activity is found in the waking EEG of infants and young children, but is abnormal in adults. Factors which cause an increase in intra-cranial pressure, for instance a brain tumour, are linked with the presence of Delta waves. They are also present in Stage 4 sleep (slow-wave sleep) and unconsciousness (Lindsley & Wicke, 1974).

 

THETA

This term was also introduced by W.G. Walter (1953). Theta waves have a frequency range of 4-7Hz. During maturation, theta predominates in all head regions, though mainly from posterior and temporal areas. The frequency is slightly higher in the frontal lobes. Theta activity is abundant in childhood and early adult life but decreases in the 20s and is abnormal beyond the age of 30. The presence of theta from the temporal regions of adults and teenagers is thought to be associated with delayed cerebral maturation and is often found in persons with severe behavioural disorders and psychopathy (Hill, 1952). Theta waves are linked with the hippocampus and limbic system (Green & Arduini, 1954) ; amplitude is usually under 20 microvolts.

 

ALPHA

Alpha activity, of a frequency range 8 - 13Hz, first appears in mid-childhood. It is prominent posteriorly over the visual cortex. Typically, it appears in bursts or 'spindles' of 20-100 microvolts. Lindsley (1938, 1939) found the mean frequency from a large adult population to be 10.2Hz. Its frequency may vary by about half a cycle, however in hypothyroidism for instance, the frequency is much reduced. In fevers, the frequency may be elevated one or two cycles.

There is much individual variation in the amount of alpha present in the waking EEG. A few persons show virtually continuous alpha ('P' type of Golla, Hutton & Walter, 1943) ; a minority have little or none ('B' type of Davis, 1941). Most people fit between these two extremes.

The generator sites are not yet known (Andersen & Andersson, 1968). The activity is stronger over the sensory and associated areas of the posterior cortex but is also present over frontal regions. It has an underlying pacemaker mechanism in the thalamus which is linked to the ascending reticular activating system. Sensory input of any kind can de-synchronise alpha - this is termed 'alpha-blocking'. Lindsley & Wicke (1974) state that alpha is sensitive to unexpected sensory stimuli, to factors which modify the state of arousal and alertness or vigilance and events which elicit or demand specific attention whether they be external events or internal events such as thoughts, ideas, worries, etc. A laterality effect or asymmetrical effect is observed I about 30% of adults i.e. one hemisphere has a greater amplitude - usually the right or 'dominant' hemisphere (Cobb, 1963). In recent years, the volitional control of alpha using biofeedback methods has become popular (Kamiya, 1962, 1967, 1969 ; Hart, 1967).

 

BETA

This common low-voltage (usually under 20 microvolts) activity of frequency range 14 to 30Hz is prominent from the frontal lobes during adulthood. Their study has been much neglected (Lindsley & Wicke, 1974). Jasper & Penfield (1949) found that in a patient with an exposed part of the motor cortex, beta waves at local regions could be blocked by voluntary effort.

 

GAMMA

Jasper & Andrews (1938) divided up the beta activity described by Berger (1929) as 20-50Hz into beta waves of 14-30Hz and gamma waves of 30-50Hz.

 

KAPPA

Kennedy, Gottsanker, Armington & Gray (1948) found a frequency similar to alpha (8-12Hz) of about 20 microvolts at the temples, which seemed to be associated with intellectual activity. The bursts of kappa are supposed to increase with reading, memory and arithmetic tasks, and problem-solving. Not all subjects evince the waves, but Chapman (1972) suggests that where present it is a reliable effect.

 

MU

Gastaut (1952) described this 9-11Hz rhythmic bursts of which appear in the EEG of about 7% of subjects (Other names are : 'comb', 'wicket', 'rythme en arceau') : It is rare after the age of 30. It is found in the Rolandic area, usually bilaterally asynchronous. The rhythm is apparently decreased by movement or intention to move the contralateral limb.

 

LAMBDA

These are single positive waves of 'sawtooth' appearance (over 250mS) recorded at the occiput in some people (Gastaut, 1951 ; Evans, 1952). They seem to be linked with visual perception.

 

VERTEX WAVES

These are single sharp negative waves (generally under 25 microvolts) over the vertex. They occur randomly - especially in children (Gastaut, 1953) ; 20% of normal adults show them (Roth, Shaw & Green, 1956).

The electro-oculogram (EOG) is a recording of eye-movements obtained from electrodes placed usually above and under the outer canthus of each eye. The electrode arrangement can be varied according to the type of ocular activity being studied e.g. vertical, horizontal or oblique movements. The electrodes pick up potentials caused by movements of the dipole moment of the electrical charge on the retina and cornea of the eye. The cornea is positive (by 1 millivolt) relative to the retina because of the higher metabolic activity of the latter (Greenfield & Sternback, 1972).

The electromyogram (EMG) is a recording of muscle potentials. Electrodes placed over a muscle indicate the general level of tonus as well as monitoring discrete contractions (Greenfield & Sternbach, 1972).


CHAPTER II

 

II.3 HUMAN SLEEP-STAGES AND SCORING CRITERIA

Oswald (1962) defined sleep as a healthy recurrent condition of inertia and unresponsiveness. Its study was somewhat limited until all-night polygraphic monitoring of subjects was performed and the various sleep-stages discovered (Aserinsky & Kleitman, 1953 ; Dement & Kleitman 1957b). In general terms there are two sleep states : Rapid eye movement sleep (REM) and non-REM (NREM). The terminology of sleep states has varied remarkably over the years so that even totally contradictory terms refer to the same state. Freemon (1972) found 25 different nomenclatures for REM and NREM sleep states in the literature (Table II.1, page 18).

Four NREM stages have been distinguished by their different appearance in the polygraphic record. In human sleep there is a roughly 90 minute cycle during sleep in which the different stages appear sequentially.

Typically, the subject enters NREM stages 1 through to 4, then reverses back to stage 2, after which stage REM occurs. This pattern is repeated several times throughout the night, but the amount of stage 4 decreases each time and the duration of the REM state increases (Figure II.2, page 19).

Rechtschaffen & Kales (1958) published a manual for scoring sleep stages so as to standardise scoring criteria. The authors suggested, among other things, a minimum chart speed of 10mm/sec for clear identification of EEG frequencies, a minimum time-constant of 0.3 secs and a minimum pen deflection of 7.5 - 10mm for 50 microvolts. EEG monitoring from positions C4/A1 or C3/A2 (according to the 10/20 system) was proposed. In EMG recording, high amplification is suggested (20 microvolts or higher) with a fast time-constant to eliminate slow potentials from other sources which could cause amplifier blocking at high gain. Records are scored by judging which sleep stage is present on each page (epoch) - usually of about 20-30 seconds ; this judgement sometimes depends on preceding or following epochs. The total percentage of the different stages can then be computed.

The sleep stages are :

STAGE 1 :

This stage occurs first when falling asleep, or after gross body movements in sleep. The EEG is low-voltage mixed-frequency activity, with many 2-7Hz waves. In its latter part, vertex sharp waves may occur. There are often large slow rolling eye-movements in the EOG. The EMG level is usually lower than that of relaxed wakefulness (Roth, 1961).

 

STAGE 2 :

This stage has 'k-complexes' (Loomis et al, 1938) and/or sleep-spindles present, but the EEG amplitude is still generally low (under 75 microvolts). A k-complex is an EEG wave having a sharp negative front followed by a positive component : for scoring purposes it should exceed 0.5 secs. They occur in response to sudden external stimuli - but may also occur spontaneously (Johnson & Karpam, 1968).

Sleep-spindles are bursts of 12-14Hz activity occurring often with a k-complex.

 

STAGE 3 :

This stage has been arbitrarily defined as one in which the EEG shows a minimum of 20% and maximum of 50% f 2Hz or slower waves (delta) having an amplitude of at least 75 microvolts peak-to-peak. K-complexes and spindles may be present in stage three.

 

STAGE 4 :

Here, the EEG record shows 50% or more of 2Hz or slower waves with a minimum amplitude of 75 microvolts ; sleep-spindles may or may not occur.

 

STAGE REM :

The EEG here is of low-voltage mixed frequency, like that of Stage 1, with - very often - distinctive 'saw-tooth' waves (Schwartz & Fischgold, 1960 ; Berger, Olley & Oswald, 1962). Alpha is usually a little more prominent than in stage 1

But the frequency is slower by 1-2Hz than during wakefulness (Johnson, Nute, Austin & Lubin, 1967). No k-complexes or spindles are present in stage REM. A main characteristic is the presence of episodic REMs. Stage REM sleep is not so scored if mental-submental muscle tonus is high in the EMG (Berger 1961 ; Jacobson, Kales, Lehman & Hoedemaker, 1964). Complicated and specific rules for scoring stage REM under all conceivable conditions are stated in the sleep-manual of Rechtschaffen & Kales (1958).

The basic electro-physiological criteria of sleep having been stated, in the next chapter an overall view of general sleep-research findings will be reviewed to illustrate the nature of sleep and the various experimental approaches.

 

(Keith Hearne's PhD thesis, pages 17 - 21)

Page 17 : Figure of the 'ten-twenty' electrode system of electrode placement

Page 18 : List of nomencalture of sleep stages

Page 19 : Figure of typical night of sleep in a young adult (sleep stages)

Pages 20 - 21 : Figure of EEGs of different sleep stages.


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.1 THE PHYSIOLOGY OF SLEEP

 

Numerous physiological changes are correlated with sleep, reflecting the alteration in level of metabolism associated with the rest / activity cycle. Body temp­erature is affected by metabolic rate (measured by oxygen consump­tion or rate of heat-loss). In sleep, oxygen consumption falls off gradually reaching a nadir after some 6 hours : at that point the curve shows a small inflection (Brebbia & Altshuler, 1965) ; rectal temperature shows a similar decline curve (Kreider, Busirk & Bass, 1958). Pulse rate begins to decline before sleep when the body is fairly inactive and falls sharply at first (Schaff, Marbach & Vogt, 1962). Respiratory depression is another characteristic of sleep and the expired air contains increased levels of carbon dioxide (Kleitman, 1963 ). These metabolic measures are usually quite stable in NREM sleep, but fluctuations are apparent in Stage REM (see p 24 ). Basal skin resistance appears to alter too throughout the night ; workers have reported that resistance increases i.e. conductivity is decreased (Farmer & Chambers, 1925 ; Batini, Fressy & Coquery, 1965). Landis (1927) attrib­uted this to drying of electrodes and polarisation. Other exper­imenters have reported different curves depending on whether a continuous or intermittent current was used (Wenger, 1962 ; Tart, 1967). This measure therefore remains controversial ; studies of blood-pressure in sleep have been inconclusive for the technical reason of accompanying sleep disturbance. Generally though, there is evidence that systolic pressure is positively correlated with depth of sleep (Snyder & Scott, 1972 ). Plethysmographical studies have shown that vascular dilation of the hands and feet occurs during sleep (Howell, 1897; Johnson & Lubin, 1967).

Body movement is limited during NREM sleep although motility is higher in Stage REM. Overall, the number of movements increases slowly after the first hour or so (Snyder & Scott, 1972 ). Kleitman, Cooperman & Mullin (1933) reported that a person may make 20-60 postural re-adjustments during the night, but these total a mere 3-5 minutes. Brazier & Beech (1952) found that 6 minutes before a movement, cardiac acceleration occurs. During movement the EEG becomes less synchronised. Auditory thresholds are lowest after a movement and highest some 16-20 minutes later (Mullin, Kleitman & Cooperman, 1937). Motility decreases with 'depth' of sleep although much individual variation is found (Cathala & Guillard, 1961 ; Rohmer, Schaff, Collard & Kurtz, 1965). Lienert & Othmer (1965) stated that emotionally stable persons have more body movements than unstable subjects.

The physiological and psychological phenomena of REM sleep are so distinct that the Stage is now con­sidered by many to constitute a separate third State, along with NREM sleep and wakefulness (Oswald, 1962 ; Dement, 1974). Aserinsky and Kleitman (1953) observed that pulse and respiration are gener­ally higher in REM than NREM sleep. Further, much variability occurs in REM (Batini et al. 1965 ; Snyder, Hobson, Morrison & Goldfrank, 1964). Blood pressure behaves in a similar manner (Khatri & Fries, 1967 ; Snyder, Hobson & Goldfrank, 1963). Mean increase of these measures in REM sleep from the mean NREM level, was 50% (Snyder & Scott, 1972). Fluctuations also are seen in plethysmographic pulse amplitude and finger skin-temperature (Snyder, 1967), however the Galvanic Skin Response (GSR) and basal skin resistance remain relatively more stable in REM than NREM sleep (Asahina, 1962). The pupil, an index of autonomic activity when awake, remains constricted during sleep and REM (Rechtschaffen & Foulkes, 1965). Brain temperature, which stays fairly constant in NREM sleep, increases significantly in Stage REM sleep (Kawamura & Sawyer, 1965). In males penile erections are associated with Stage REM (Ohlmeyer, Brilmayer & Huellstrung,1944) ; Fisher, Gross & Zulch (1965a) found evidence that the phenomenon is not affected by sexual gratif­ication. Karacan, Goodenough, Shapiro & Starker (1966) found, though, that if Stage REM is prevented by wakening, the erection cycle appears in other Stages at the expected times i.e. in the 90 minute cycle. A phenomenon associated with the phasic REM bursts is activity of the stapedius muscle of the middle ear (Baust & Rohrwasser, 1964). In REM sleep (but not NREM) bodily paralysis is present, as indicated by EMG suppression. Actively induced tonic non-reciprocal motor inhibition occurs which blocks the frenzied activity of the brain during REM (Dement & Mitler,1974). Only small twitches are observed occasionally. Electrically induced reflexes are suppressed in REM indicating active motor inhibition (Hodes & Dement, 1964 ; Pompeiano, 1965, 1970), Tendon reflexes are abolished and voluntary movement is impossible. Sometimes, a person may wake from Stage REM to find the body paralysed (Sleep-paralysis, page 47). Bremer (1974) remarks that the state of paralysis resembles the 'apparent death' of lower vertebrates and that perhaps nature uses this archaic inhibitory apparatus for protection of the dreamer.


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.2 THE CHANGING CONCEPT OF SLEEP

Early ideas of sleep inclined to a 'passive' theory that sleep occurs to prevent fatigue or is caused by a lack of sensory stimulation (Claparède, 1908 ; Coriat, 1912). 'Active' theories also appeared i.e. that the brain actively inhibited consciousness. Pavlov (1923) thought that sleep was the result of cortical inhibition spreading from certain areas, and Hess (1931) discovered that cats could be put to sleep by electrical stimulation of the diencephalon. Bremer (1935) invoked the passive notion to explain his finding that the cerveau isolé cat (having a cut through the upper mid brain) remained in virtually continuous sleep. He thought the animal was not receiving enough sensory stimulation to keep awake. In encéphale isolé animals (where the cut is in the lower mid-brain) the sleep-wake cycle persists (Bremer, 1935). Thus, the sleep mechanism seems to be located between these brain areas. Moruzzi & Magoun (1949) discovered that electrical stimulation of the reticular formation roused a sleeping or anaesthetised cat. 'Reverberating loops' were supposed to keep the animal awake in the absence of stimulation (Magoun, 1952).

It became generally accepted that the reticular formation stimulates the cortex to consciousness. Sensory information from the sense organs is routed to the cortex whilst collateral afferents from these nerves link with the reticular formation. Lesions of the pathways to the cortex do not cause sleep, whereas lesions between the reticular formation and the cortex do (Lindsley, Schreine, Knowles & Magoun, 1950). Apparently, impulses from the collateral afferents excite the reticular formation to send diffuse 'activating' impulses to the cortex, so maintaining wakefulness.

There seems to be an inherent rhythmic sleep-wake cycle in the upper reticular formation but wakefulness is aided by external sensory stimulation (Oswald, 1962). Animals without sense organs tend to sleep excessively (Hagamen, 1959). Several factors assist in maintaining wakefulness by stimulation of the reticular formation, the 'gating' function of which controls consciousness. For instance, a decrease in blood oxygen content stimulates chemoreceptors in the carotid body which in turn stimulate the reticular formation. An excess of carbon dioxide in the blood also causes mid-brain stimulation (Bonvallet et al, 1955). Hypothalamic thermodetectors can affect the reticular formation too (Hagamen, 1959), and various influences may also diminish mid-brain activity, so promoting sleep. Baroreceptors in the carotid sinus and aortic arch dampen the reticular formation (Bonvallet, 1955). Heating of the hypothalamus encourages sleep unless excessive (Euler & Söderburg, 1957.) The cerebral cortex itself is capable of influencing the organism’s own state of wakefulness (Hugelin & Bonvallet, 1957a,b ; 1958). Worries can keep a person awake and Cannon (1942) stated that in primitive cultures (eg Aborigines) sudden death can occur in persons on the receiving end of meaning­ful symbolic acts (eg pointing a bone). Obviously, networks of feedback loops operate between the activating reticular formation and the cerebral cortex.

Not everyone subscribes to the concept though ; Freemon (1972) states that stimulation of the brain stem near the reticular formation can lead to slow waves ; this is the opposite of the Moruzzi and Magoun finding.

Freemon also says that the reticular formation does not project diffusely to the neocortex, but to the limbic areas and orbito frontal cortex, returning then to the reticular formation (Scheibel & Scheibel,1967.) Hippocampal arousal (shown by de-synchronisation of the EEG) occurs several seconds before neocortical arousal on external stimulation in NREM sleep (Freemon & Walter, 1970). Some argument exists therefore over the notion of the reticular formation’s direct involvement in causing sleep.


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.3 DEVELOPMENTAL ASPECTS OF SLEEP

Differences have been discussed between sleep EEG waveforms for different ages (II.2.(b)). Studies of premature babies show that a virtually constant EEG pattern exists before full-term (Parmalee & Wenner, 1967).

Slow waves do not become evident in the sleeping EEG, along with spindles and K-complexes, until 3 months of age, although Stage REM is present at birth and may constitute 50% of the 16 hours or so daily sleep for the first few weeks (Gibbs & Gibbs, 1950b).

The total amount of sleep and the relative amount of REM decrease steadily until approximately 4 years of age after which it varies within some 2-3% over the years, averaging about 2-3% (Roffwarg, Dement & Fisher, 1966). Kales, Kales, Jackson, Po & Green (1967) found 30% Stage 4 and 29% Stage 3 in children compared to 11% and 10% respectively for young adults.

Significant changes in the distrib­ution of sleep also occur in the early years of life. The new-born baby has 5 or 6 periods of wakefulness which reduces to 3 or 4 by 6 months (elimination of night feeding is probably responsible Kleitman 1939). At 1 year most infants have a solid 12-14 hour sleeping period with some day sleep (Gessel & Ametruda, 1945.) Thus, early polyphasic sleep is altered by socialisation and maturational factors to a monophasic form. No sex differences appear to exist between the various sleep Stages in young adults (Williams, Agnew & Webb, 1964, 1966).

The main change in EEG of the aged is gradual loss of Delta activity (Agnew, Webb & Williams, 1967 ; Kales, Jacobson, Kales, Kun & Weissbuch, 1967) although this could reflect a reduced need for deep sleep. The percentage of Stage REM in the sleep of aged persons has varied in different studies. Feinberg, Koresko & Heller (1967) found over 20% Stage REM, whereas Lairy, Cor-Mordret, Faure & Ridjanovic (1962) give a figure of 14%. However, old persons often take 'cat-naps' during the day which may affect the natural sleep pattern - thus a polyphasic dist­ribution of sleep may recur.


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.4 THE PHARMACOLOGY OF SLEEP

The two states of sleep (NREM & REM) appear to be governed by different neurochemical systems. Injections of 5-hydroxytryptophane (5-HTP) (a precursor of 5-HTP or serotonin) in cats causes NREM sleep (Jouvet, 1967). Injections of reserpine in cats suppresses both states, but subsequent injections of 5-HTP selectively restores NREM sleep (Matsumoto & Jouvet, 1964 ). Parachlorphenylalanine (p-PCA) selectively blocks 5-HTP synthesis, and Weitzman, Rapport, Mc Gregor & Jacobs (1968) discovered that when injected into monkeys it decreased the amount of sleep by reducing NREM sleep : REM sleep was unaffected. Significantly, anaesthetics increase the amount of serotonin in the brain (Freemon, 1972). Thus, 5-HT appears to be important regarding the presence of the NREM state.

It is possible that the cholinergic system however is important for the production of REM sleep. For instance, the REM state is enhanced in cats by carbachol (a cholinomimetic) and reduced by atropine (a cholinergic blocking agent. In addition, injections of acetylcholine near the locus coeruleus trigger REM sleep in cats (George, Haslett & Jenden, 1964). Jouvet (1969) though, implicated the nor-adrenaline system in the control of REM sleep. Thus, after depletion of nor-adrenaline by reserpine, Dopa (a nor-adrenaline precursor) restored REM sleep (Matsumoto & Jouvet, l964 ). The paradoxical finding that persons are hard to rouse from REM sleep (despite the high cortical arousal) could be supported by assuming the nor-adrenaline system is involved in behavioural arousal and that the ascending nor-adrenaline pathways are inactive during REM sleep. Jouvet (1967) thought a link existed between the nor-adrenaline system of the pontine part of the brain stem (ventral and caudal to the locus coeru1eus) and ponto-geniculo-occipital spikes occurring in the EEG of cats. Jouvet considered that dreams may be initiated by PGO spikes produced by the release of mono-amines at this site. Perhaps both neurotransmitter substances are operating in Stage REM.

Hypnotics affect the cerebral cortex, the reticular formation or the medulla. Anxiety, causing insomnia may be treated by tranquillisers such as chlordiazepoxide (Librium). Depression, which often results early morning wakening is often alleviated by antidepressants e.g. amitriptyline (Laroxyl), or trimipramine (Surmontil). This latter drug does not decrease REM or result in a rebound effect (Oswald, 1974 ). Pain which prevents sleep can be treated with morphine or pethidine. The barbiturates are the most effective soporific drugs in use. Unfortunately they are lethal in overdose and can interact with other drugs : they are also addictive (page 44). It is not known exactly how barbiturates work except that they produce widespread inhibition in the cortex. They are either 'long-acting' (e.g. phenylbarbitone) or 'short-acting' (e.g. quinal-barbitone). Newer drugs have appeared, such as the benzodiazepines (e.g. Mogadon) or flurazepam (e.g. Dalmane). These drugs suppress the reticular formation and overdose is not fatal since the medulla (controlling breathing) is not affected. The famous 'Micky-Finn' consisted of alcohol and chloral. A modern version is dichloralphenazone (Welldorm). Sleeping tablets frequently lead to many problems. Dement & Villablanca (1974) stated that "with one or two exceptions, all sleeping pills will always cause or worsen insomnia".


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.5 SLEEP DEPRIVATION

Some persons claim to require little or no sleep (Jones & Oswald, 1968 ; Meddis, Pearson & Langford, 1973), however, for most people total sleep deprivation leads after several days to visual illusions and hallucinations, speech slurring, inability to concentrate and memory lapses (Ross, 1925 ; Kollar, Namerow, Pasnau & Naitoh, 1968 ; Cappon & Banks, 1960 ; Bliss, Clark & West, 1959 ; Morris, Williams & Lubin, 1960). Paranoid symptoms may also occur in some subjects (Tyler, 1947, 1955). Boring test sit­uations produce, not surprisingly, the lowest performance scores in sleep deprived subjects. Thus, such persons, when told to signal when they observed a light spot at any one of 8 points on a screen, over 40 minutes, performed steadily worse though watching the screen (Wilkinson, 1960). During auditory tasks errors of omission occurred with the loss of alpha rhythm (Williams, Lubin & Goodnow, 1959). Oswald (1962) attributed such phenomena to falls in cerebral vigilance. Mental capac­ities can be improved temporarily to waking levels on some tasks if subjects can take their time and amend mistakes.

The EEG of sleep deprivation shows a decrease in the alpha rhythm of relaxed wakefulness (Tyler, Goodman & Rothman, 1947). Additionally, biochemical changes occur, probably due to lack of restoration which mostly occurs in sleep. Plasma iron level and plasma cholesterol both decline (Kuhn, Brodan, Brodancva, & Friedman, l967). Amphetamines temporarily improve the perform­ance of sleep deprived subjects on rote tasks (Weiss & Laties, 1962).

On the first recovery night after sleep deprivation a marked increase in NREM sleep is observed (Berger & Oswald, 1962 ; Williams, Hammack, Daly, Dement & Lubin, 1964), whilst the REM percentage remains the same (Kales, Tan, Kollar, Naitoh, Preston & Malmstrom, 1970). On subsequent nights REM sleep is higher. Thus, NREM sleep has priority in the recovery process. Studies have been conducted on the selective suppression of REM sleep by means of waking the subject at its onset, or pharmaceutically by drugs which suppress the state. A remarkable finding is that a 'rebound' effect occurs when uninterrupted sleep is once again permitted. In the case of drugs (most suppress REM), a sharp decrease in the percentage of REM is seen at first. Gradually, the percentage rises to normal, due to physiological tolerance. On cessation of the drug, a rebound occurs (and the amount is larger than by selective awakenings) so that it amounts to 150-200% of the loss. A 'need to dream’' has been postulated on such evidence. Early studies suggested that REM deprivation led to profound psychological changes such as irritability (Dement, 1960), extreme hunger (Dement & Fisher, 1963), and oral behaviour with oral symbolism (Fisher, Gross & Zulch, 1965c). However, Kales, Hoedemaker, Jacobson & Lichtenstein(1968) failed to detect any psychological alterations with long term REM deprivation. Also, depressed patients are not adversely affected by REM deprivation (Vogel, Traub, Ben-Horin & Meyers, 1968) neither are schizophrenics (Vogel & Traub, 1968). Indeed, mono-amine-oxidase-inhibitors (MAOI) which apparently totally suppress REM do not cause abnormalities (Wyatt, Fram & Kupfer, 1971).


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.6 MEMORY AND SLEEP

Jenkins & Dallenbach (1924) found evidence that rote-learnt material was recalled better after 8 hours of sleep than wakefulness, presumably because of the lack of interference by subsequently learnt material. Empson & Clarke (1970) discovered that REM sleep seems to be important for the consolidation process. 20 yoked pairs of subjects listened to tapes of nonsense phrases before bed. One subject was later chosen to be REM deprived, by waking. At that time the other subject was woken too. The Experimental subjects showed less recall than the Control subjects woken at random sleep Stages.

The idea of 'sleep-learning' whereby auditory information is supposedly absorbed and consolidated in the absence of wakefulness is popularly believed to be an estab­lished effect. However, Simon & Emmons (1956, 1956a) discovered failings in methodology in such work. They used all-night EEG monitoring on 21 subjects. After establishing their baseline general-knowledge, they presented each of 96 questions and, 5 seconds later, the answer. Subjects had to call out if they heard an answer during sleep. Subjects were tested the next day to see if they could recall the answers. When subjects were awake (showing alpha blocking) at the original presentations, recall was very good - when drowsy (alpha present) recall was not so good (50%). Recall was minimal otherwise. The authors also tried repeating stimuli - in the form of 10 one-syllable numbers (Emmons & Simon, 1956b). The Experimental subjects performed no better than Controls. It therefore appears that memory traces (engrams) are not laid down during sleep.


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.7 EXTERNAL STIMULI AND SLEEP

External stimuli can affect a sleeping person. In Stage 2 of NREM sleep a sudden sensory stimulus causes the appearance of a 'K-complex' in the EEG (Davis, Loomis & Harvey, 1939 ; Roth, Shaw & Green, 1956).The size of the response appears to be related to the meaningfulness of the stimulus (Oswald, Taylor & Treisman (1960) found that subjects responded more to their name being called than other names or to their name being played backwards.

In REM sleep external stimuli may be incorporated into dreams reported on waking. Berger (1963) found that spoken names were included - often in a distorted fashion. Thus, 'Naomi' became 'an aim to ski', and 'Jenny' became 'jemmy'. Dement & Wolpert (1958) tried stimulating subjects with a tone, light and water-spray. They found the incorporation amounted to 9%, 23% and 42% respectively. Koulack (1969) used an electrical stimulator positioned on the median nerve at the wrist and obtained direct incorporation in 40% of cases and indirect in 24% , when the stimulus was applied 3 minutes after the start of the REM and where wakening occurred 3 minutes after stimulation.


CHAPTER III

GENERAL SLEEP-RESEARCH FINDINGS

 

III.8 SIGNALLING FROM SLEEP

Several studies have claimed to show that animals and humans can make movements or signals (motor acts or speech) from the 2 states of sleep. The movements though are of a simple repetitive kind, or single responses to stimulation, not requiring higher processing. Oswald (1959c, 1960a) had subjects moving arms and legs rhythmically to music with eyes closed or taped open. The movements continued but less vigorously with the cessation of alpha rhythm, but sometimes movements ceased. Defensive and reflexive movements may occur in sleep, but these are also found in decorticate animals (Kleitman & Camille, 1932).

Vaughan (1963) used macaca monkeys in an experiment to test whether they could respond (by pressing a bar) to imagery in sensory isolation as they had previously been tra