Sleepy sickness

A hare which started with my re-reading the book at reference 1, after getting on for twenty years, jumping from there to reference 2 and from there to reference 3, this last a paper dating back to 1930. The author then being Professor of Psychiatry and Neurology at the Clinic for Psychiatry and Nervous Diseases in the General Hospital in Vienna. A paper, presumably written in English as the author was good at languages, read before the College of Physicians and Surgeons at Columbia University, New York, on the 3rd December, 1929. A paper arranged in two columns, with no headings or sub-headings, with just one crude diagram, no tables and no references. Not even a number, never mind a statistic in sight. Wouldn’t do these days at all.

The time of the epidemic of encephalitis lethargica, mixed up with the roughly contemporary pandemic of Spanish influenza. An epidemic which perhaps touched a million people and killed half of them. What is now thought the be just the most recent and most serious such outbreak, with now-suspected outbreaks going back to the sixteenth century. A disease which, according to reference 6, remains poorly understood to this day. With the lack of new material being good for potential victims, bad for science. Victims which have previously been noticed here, at reference 5.

The present author being among the first to properly identify and describe the disease, a disease which involved severe disturbances to sleep patterns and which led him to take an interest in finding out from where in the brain sleep was controlled. One result being the present paper.

He starts by surveying various theories accounting for sleep, the regular alternation between waking and sleeping exhibited by all mammals. Even mammals without most if not all of their cerebrums. With natural sleep being easily interrupted, which is not the case, for example, with anaesthetics.

Some theories proposed the more or less mechanical blockage of nerve signals, with one suggesting that the dendrites of neurons were withdrawn during sleep, more or less shutting down their synapses with other neurons and so shutting down neural activity. Sleep was the result of the higher levels of the brain no longer being stimulated. A theory seemingly corroborated by old and new experiments on sensory deprivation, with, as I recall, a common reaction to entry to the deprivation chamber being to fall asleep, and to stay asleep for hours. 

Other theories had a more chemical flavour, perhaps involving a steady increase of substance X in the waking state, an increase which eventually triggered a reaction in the form of sleep which made space for the level of X to come down. We are told of an experiment in which ‘the blood serum of dogs which had overexercised for several days, and were not allowed to sleep, produced prompt sleep when injected into healthy dogs which had had sufficient sleep. That proved that fatigue produces substances in the blood which may provoke sleep’. But as the author points out, such a substance X does not of itself explain how it is that we can fall asleep when we are not tired or the ease with which we can usually be woken up.

And for periodicity, we are reminded of the many systems in our body – one of which being the ovulation cycle of younger women and another being the beating of the heart – which require some kind of a clock. The machinery is there.

But, quibbles aside, the chemical theories looked to be on the right track. The next question was from where was this chemistry being run? With many thinking that it was not localised, that there was not a sleep control centre. Which was where the matter stood when the epidemic of encephalitis lethargica came along in the middle of the first world war.

With the author being the first, or at least one of the first, to recognise that the part of the brain which was being damaged, with one of the symptoms being massive disturbance of sleep patterns, was the upper brain stem. Another symptom was disturbance  of motor activity, disturbances which were rather like those observed in those suffering from Parkinson’s. Plus disturbances of the muscles which controlled the eyes.

One of the disturbances of sleep was its disconnection from motor inhibition. Patients’ arms and legs might be awake when their brains were asleep, and vice-versa.

The author points to other diseases, which affect the same part of the brain and which also affect sleep.

He goes on to suggest that  ‘… this experimental fact suggests that normal cerebral sleep might be considered as an inhibitory action brought about by the center of sleep regulation upon the cerebrum and thalamus…’. A centre which, as it happens, is very near the centres which control the bodily functions which need to be modulated for sleep. Which does not seem so far from Hobson’s position, as set out in reference 1, 70 years later.

A centre which might well respond to excess substance X (above) by firing up some inhibitory neurons, but which might also allow those neurons to be stopped when someone went to wake the subject up. Thus allowing for reversibility in a way that substance X alone does not.

He closes by suggesting that further work to further localise the sleep centre may open the door to more sophisticated treatments for sleep disorders than were available at the time of writing.

More on sensory deprivation

Von Economo mentions the case of a patient of one Adolph von Strümpell - a neurologist active a little over a hundred years ago - who had lost all tactile sensation and who fell asleep when his ears were blocked and he shut his eyes. The best I was able to turn up was reference 12 where we have:

‘… Consider the patient described by Adolph von Strümpell (1853–1925): totally anaesthetic, completely deaf and blind in one eye, he sleeps and is unconscious whenever the one good eye is shut….’.

Which may well not be the same patient, but the force of the example is the same: shut down all sensory input and the subject will sleep. But Von Economo was not satisfied with this. It was not the whole story and he wanted more.

I failed to trace the study on sensory deprivation that I remember reading years ago. But what I remember is an isolation room, with little or no light and little or no sound. There was a bed, on which the occupant was presumed to spend most of his or her time. Bodily needs were dealt with as unobtrusively as possible. The idea was that volunteers stayed in this room for several weeks. Part of the interest was seeing how their sense of time and date behaved over time – with one volunteer not playing the game at all and making a pendulum out of a bent paper clip or something. But one could hardly watch a pendulum for days on end and I forget how that translated into successful time keeping. The bit that is relevant here, is that a good proportion of the volunteers went to sleep shortly after entry and stayed asleep for hours, eventually returning to more normal sleeping patterns. Further support for the idea that when all external stimulation is withdrawn, the subject relaxes to the point of falling asleep.

I do not see a problem with all this; it does not bear on the remainder of Von Economo’s argument.

Then coming at isolation from the body clock point of view, a number of intrepid researchers have lived for months in caves and suchlike where there is no natural light. But body clocks were the subject of this work and I do not recall the sleep angles, if any.

Plenty of work seems to have been done with isolating flotation chambers, where the subject floats in a warm salt bath, presumably a bit like a warm, dark version of floating in the Dead Sea. But spells in these chambers are (necessarily) of much shorter duration, an hour or two, perhaps as long as a day, rather than weeks at a time. Some of this work has been performance art and more of it has been to see whether it helps with addictive behaviours. Sometimes called ‘Restricted Environmental Stimulation Therapy’ or REST. See, for example, references 7 and 8. And there plenty of alternative therapies based on same: they even make it to ‘Midsomer Murders’. But the format does seems to be hours rather than the weeks that I remember.

Most people seem to find these chambers very relaxing – rather than claustrophobic – and it seems to me quite likely – without ever having tried such a thing – that one would go to sleep – but this is not what seems to be happening.

I wonder now whether going into a deprivation chamber with the idea of staying there for a good while, perhaps for weeks, is a different proposition than just going in for an hour or so. Given that it is all very relaxing, you can just yourself go. Plenty of time for other stuff later on, should one feel the urge. For now just go with the flow. 

All in all, while sensory deprivation is a long way from being a sufficient explanation of normal sleeping, there does seem to me to be a connection worth exploring. Maybe I have just failed to find the reports from the explorers.

Aside: Suedfeld points out in reference 8 that while solitary confinement in prisons minimises personal contact, it does not reduce the totality of external stimulation as much as one might at first think. Most prisons, for example, are very noisy places. Suedfeld also points to the bad press that sensory deprivation got in the 1960’s and 1970’s, being thoroughly mixed up with the brainwashing scare on the one hand and the sort of interrogation techniques then being deployed in Northern Ireland on the other. See references 10 and 11. I have not been able to find a free copy of the latter.

Other matters

According to Wikipedia at reference 4, the German neurologist Felix Stern, important between the wars in the world of lethargica, thought, without any proper evidence, that lethargica was in some way related to polio. It now turns out that the former might be caused by something called an enterovirus, which poliomyelitis (aka polio)  certainly is. So there is a connection of sorts. With an enterovirus being one that usually gets in through the guts but which can also live in the lungs. While other theories are built on disturbances of the immune system.

Von Economo mentions sleeping plants in a couple of places, in support of the argument. On investigation, this appears to be the plants which open and shut their leaves and flowers with the coming and going of the sun. One might be interested in how exactly plants do this, but I don’t think it has much to do with the sleeping arrangements of higher animals.

Slightly frivolously, I am reminded of the fact that if one has 100 fortune tellers, is it reasonably likely that one of them will turn out to have got it right, without any of them having had any special powers. Something to do with the law of large numbers.

I was interested to read at reference 8 of the difficulties of coming up with good ways to classify the outcome of treatments to get people to stop smoking. Even such a simple sounding outcome comes with all kinds of statistical classification baggage.

I have taken the occasional peek at reference 9 to keep me on the straight and narrow – remaining of the view that there are ideas there which are still of value. The idea, for example, that some kind of censorship is going on when material is being propelled towards consciousness.

Conclusions

Old paper are sometimes not so wide of the mark – and sometimes they can even be useful reading today.

That said, Von Economo was backing the very top of the brain stem as his sleep centre, just below the third ventricle in the figure above. While I think Hobson is backing a slightly lower region, in and around the pons.

References

Reference 1: Dreaming: An introduction to the science of sleep – J. Allan Hobson – 2002.

Reference 2: REM sleep and dreaming: towards a theory of protoconsciousness – J. Allan Hobson – 2009.

Reference 3: Sleep as a problem of localization – Von Economo, C. – 1930.

Reference 4: https://en.wikipedia.org/wiki/Encephalitis_lethargica.

Reference 5: https://psmv4.blogspot.com/2018/12/awakenings.html. An earlier outing for encephalitis lethargica, and the film about same based on a book by Oliver Sacks. A mention of body clocks coming unstuck.

Reference 6: Encephalitis lethargica: 100 years after the epidemic - Leslie A Hoffman, Joel A Vilensky – 2017. From the Indiana University School of Medicine, Fort Wayne, Indiana, USA. Open access.

Reference 7: Sensory Deprivation – Till Bödeker – 2020. A performance artist interested in sensory deprivation – one who has given us a first person account of what sensory deprivation is like.

Reference 8: Restricted Environmental Stimulation and Smoking Cessation: A 15-Year Progress Report - Peter Suedfeld – 1990. An eminent Hungarian-Canadian professor of psychology.

Reference 9: The interpretation of dreams – Sigmund Freud – 1899/1954.

Reference 10: Public psychology and the Cold War brainwashing scare – Dr. Charlie Williams – 2020.

Reference 11: The Ulster depth interrogation techniques and their relation to sensory deprivation research – Shallice T. – 1972.

Reference 12: The evolution of consciousness. Together with a diagram illustrating certain homologies in the nervous system. By W.H.B. Stoddart MD MRCP. Brain 1903; 26: 432–439. With The structure of consciousness by Michael Polanyi. Brain 1965; 88: 799–810 – Alastair Compston – 2017.

Reference 13: https://www.earthslab.com/anatomy/third-ventricle/. The source of the opening snap.