An apnoea is a cessation of breathing. When sufferers of sleep apnoea enter deep sleep, their airway becomes blocked by the tissues around their throat. They may gasp for air, and stir hundreds of times a night to a level just below conscious awareness. People with sleep apnoea wake up in the morning feeling as if they’ve slept normally, but are chronically tired because their sleep isn’t restorative. As a medical student in the 1990s I was paid to be a subject in sleep apnoea experiments. The condition had been described not twenty years earlier, and researchers were still trying to define how debilitating it could be. I’d cycle over to a sleep lab in Edinburgh’s psychiatric hospital, have electrodes glued to my head, then be shown to a room with a bed and a one-way mirror, on the other side of which sat a researcher, watching. They didn’t tell me on which nights my sleep would be interrupted: on these test nights, whenever I drifted into a deep sleep the researcher would play sounds through a loudspeaker over the bed, raising my encephalography (EEG) reading until I was nearly but not quite awake. The next morning I would be convinced I’d slept the night through, but the tests of mental agility and hazard awareness they put me through suggested otherwise. I’d crash the driving simulator and flunk at mental arithmetic.
Sometimes it would take me hours to fall asleep. I’m prone to insomnia and having electrodes glued to my head didn’t help. Neither did knowing someone’s research depended on my reliably nodding off. They would encourage me to read in dim light before trying to sleep. I remember I had a book of Borges’s stories on the go. They didn’t help either, until I reached ‘Funes the Memorious’, which includes a portrait of the eponymous mnemonist struggling to sleep. Following a head injury Funes has developed an ‘infallible’ memory. He ‘not only remembered every leaf on every tree of every wood, but even every one of the times he had perceived or imagined it’. To fall asleep is to release oneself from engagement with the world, but Funes can’t stop his mind teeming with details. When I first tried to sleep in the laboratory I couldn’t either. The only way Funes can find rest is to call up images of oblivion, such as being embedded in black obscurity, or imagining ‘himself at the bottom of the river, being rocked and annihilated by the current’. Lying awake in the lab, keenly aware that my thoughts were producing EEG readouts for the researchers’ scrutiny next door, I tried out the same visualisations as Funes – and fell asleep.
Funes’s circumstances are as extreme and fantastical as you’d expect from Borges, but his sleeping problems are ordinary enough. It’s estimated that about 10 per cent of the world’s population suffer chronic insomnia – a symptom, not a diagnosis – and the proportion who sleep poorly is higher still. Many of my own patients spend restless nights preoccupied by the details of their day, picking over regrets, or anxious about the future. I have seen several cases of Brexit-associated insomnia. The ubiquity of advertisements for mattresses is an indication of just how many people are struggling, but uncomfortable beds aside, there are scores of interwoven reasons people have trouble sleeping. Meir Kryger’s The Mystery of Sleep takes a clinical approach to disentangling some of them.
No one can say exactly why we have to sleep, but every organism goes through alternating periods of repose and activity. Some cetaceans, seals and birds sleep with one half of their brain at a time, which is taken as evidence that sleep has a vital role in maintaining cerebral hygiene. Sleep is thought to remove waste material produced by brain cells, restore aspects of the body’s function and repair injured tissues. One of the reasons children sleep so much is that it’s during sleep that growth hormone is generated by the body. The longer we’re awake the more a chemical called adenosine accumulates in the fluid around brain cells. Adenosine is crucial for cellular energy metabolism, but too much of it makes us feel terrible: sleep returns it to its normal levels.
Different phases of sleep seem to have different functions. In slow-wave sleep, the brain’s EEG tracings show deep co-ordinated pulses in neural activity. Without adequate slow-wave sleep we may wake feeling unrefreshed. REM sleep, in which the majority of dreaming occurs, is important for memory consolidation, or perhaps the systematic forgetting of useless information. (REM stands for ‘rapid eye movement’; though the body is paralysed the muscles around the eyes continue to move.) We experience REM every ninety minutes or so while asleep – most adults have four or five episodes of it each night.
Much about the detail and the mechanisms of sleep remains mysterious. Newborn babies spend about half their sleep time in REM sleep, and adults about a quarter. The deepest phases of slow-wave sleep diminish as we age – some elderly people don’t engage in slow-wave sleep at all. REM is triggered by a tiny bunch of neurons with roots deep in the brainstem, which flow into a region at the core of the brain called the thalamus. Only mammals and birds have REM; if you wake someone during it, 90 per cent of the time they’ll say they were having a dream.
From the 1950s until the 1990s it was widely assumed that to be in REM sleep was to be dreaming, but more recently that’s been shown to be wrong. If you wake someone during slow-wave sleep, there’s a 10 per cent chance they will report a dream, though the dreams tend to be more conceptual and less vivid than dreams reported during REM. If you’re prevented from drifting into deep sleep (through exposure to sounds in a sleep lab for instance) your chances of reporting a dream when awoken from non-REM sleep rise above 70 per cent. No one can agree on the purpose or meaning of dreaming, but it looks as if Freud’s theory – that dreams are the guardians of sleep – is at least partly right: they convert external stimuli such as lights or sounds into dreams rather than waking awareness. If you suffer brain damage that prevents REM sleep you will still dream, but if you sustain damage to an area called the ventromesial quadrants you will retain the capacity for REM sleep, but it will be dreamless.
I’m a GP, not a psychoanalyst, but listening to my patients’ accounts of their dreams can on occasion be helpful, revealing preoccupations the patient can’t articulate. The title of Freud’s The Interpretation of Dreams was taken from Oneirokritika, by the second-century Ionian Greek Artemidorus. ‘To see often the same dreams, and many nights one after another,’ Artemidorus wrote, ‘is a sign that our spirit admonishes and foretells us affectionately the self same thing worthy to be thought upon.’ I appreciate the gentleness of that ‘affectionately’; some of my own consultations become shared reflections on what recurring dreams might mean. A patient with a recurring bad dream may choose to suppress it rather than try to understand it, in which case the prescription drug clonazepam often helps.
Both men and women experience increased blood flow to their genitals during dreaming sleep, even if the dreams have no sexual content. During REM most of our muscles are paralysed for good reason – so we can’t act out our dreams. Some have a behavioural disorder whereby this paralysis fails: they may attack bed partners, or throw themselves out of bed. This is different from sleepwalking (which happens during non-REM sleep) and also from night terrors – so common in young children as to be normal. There is an overlap between these conditions and the recurring nightmares that afflict some sufferers of post-traumatic stress.
If you’re severely sleep-deprived you may experience vivid dreams as you drift off or wake up (hypnagogic and hypnopompic hallucinations respectively), but to experience these routinely suggests narcolepsy, which brings on a sudden and irresistible urge to sleep. It is connected in mysterious ways to cataplexy (‘struck down’), when a muscle paralysis similar to that experienced in REM sleep is switched on in moments of elation or heightened energy. There are patients who collapse limp on hearing a joke, or when they have an orgasm.
Kryger was among the first physicians in the 1970s to recognise sleep apnoea as a syndrome. The first patient he wrote up became so oxygen-depleted while sleeping that he had seizures. The cure was radical: a permanent hole bored into his trachea (a tracheostomy), bypassing the collapsing throat tissues. Insurers won’t cover someone with sleep apnoea – they’re considered a risk on the road or while operating machinery – unless they’re undergoing treatment, which is usually less dramatic than a tracheostomy: a mask over the mouth or nose that blows air to keep the throat open while you sleep. One of the principal causes is obesity: when the fatty tissue around the throat is slimmed away the airway opens up and the syndrome is cured. Children with swollen tonsils and adenoids get sleep apnoea (it’s now one of the commoner indications for tonsillectomy), as do some slim adults with a small jaw and large tongue.
Sleep apnoea is on the increase because obesity is a disease of modernity – about two thirds of Americans are classed as overweight, and one in five worldwide are considered clinically obese. In the West we sleep around two hours fewer per day than we did a century ago because of another consequence of modern living: electric light. The bluish light emitted from screens is pernicious when it comes to disrupting sleep, because the brain interprets it as morning. To expose yourself to blue light every evening is to risk mild and persistent jetlag, as your body clock tries to adjust in response to this ‘morning light’. The sleep clinic to which I send patients in Edinburgh prescribes orange filters for the use of screens in the evening: they translate the pixillated light into the colours the brain associates with sunset and firelight.
Some sleep disorders affect not its quality, but its phase and timing. ‘Early to bed, early to rise’ isn’t a marker of moral probity, but a genetic inheritance: some people are naturally ‘larks’, others are ‘owls’, according to the ‘clock genes’ they inherit. Many years ago, as the doctor on an expedition, I studied the effect of these genes on people living through a lightless Antarctic winter. Without environmental cues like sunrise and sunset, larks could find that their body’s hormonal rhythm shortened their day to 22 or 23 hours, while the owls’ day might extend to 25 hours. To be released from the celestially ordained 24 hours is called ‘free-running’, something experienced by many blind people when their brains, also divested of light cues, cannot gauge the length of a day. Some pilots experience the same thing, because their ‘days’ change in length as they fly around the globe; they cope by sleeping on a fixed schedule.
Light suppresses the secretion of the hormone melatonin from the pineal gland, which is how the brain tells the body there’s a shape to the day. In humans the gland is buried deep between the two cerebral hemispheres (Descartes thought it was the seat of the soul). It receives its information about ambient light via nerve fibres in the retina that respond specifically to blue light. In some lower-order animals, the pineal gland is exposed near the surface of the brain, and responds directly to ambient light filtering through the skull. Melatonin pills can enable blind people to establish a diurnal rhythm, and help with jetlag. It was discovered that the best way to keep the Antarctic base running to a 24-hour clock was to set up bright lights around the base and at every workstation, and to make sure everyone had enough exposure to them in the ‘morning’. Light isn’t the only means of synchronising the body clock: scheduled meals and the timing of exercise are important too.
Kryger spends some time on Restless Legs Syndrome, which he calls ‘the most common medical problem you never heard of’. Some people can’t stop moving their legs in bed, either just before they go to sleep or even during it. For many the twitchiness is simply an irresistible urge to move, for others it is experienced as a creeping sensation over the skin. Restless legs, like insomnia, are a symptom rather than a diagnosis: iron deficiency, anaemia, vitamin deficiencies, arthritis, diabetes, renal impairment and low mood are all predisposing factors – a list broad enough to take in much of the adult population. Identifying the cause and treating it might settle the restlessness, but in many cases no cause can be found. For reasons that no one understands, the twitchiness can sometimes be cured with the same drugs used to treat Parkinson’s disease.
Some will pick up The Mystery of Sleep looking for tips on how to deal with insomnia. Kryger’s 13 ‘commandments’ will be familiar to anyone who has wearily scoured sleep hygiene checklists online. About three-quarters of people with insomnia improve with a course of cognitive behavioural therapy, which seeks to identify the thoughts and behaviours that are causing the trouble, and recast them in healthier patterns. Sleep restriction can help – getting up after six or seven hours asleep even if you don’t need to – and avoiding long lie-ins at weekends. Most sleep hygiene regimes recommend getting up after twenty minutes of lying in bed sleepless, not to watch TV but to engage in something, anything, that doesn’t expose you to too much light, and won’t be too stimulating. Kryger suggests reading something not too engrossing, ‘for example a boring history book’ or perhaps a clinical manual on sleep disorders thinly disguised as a text for the general reader. He advises partners of restless sleepers to consider separate rooms: one patient of Kryger’s saved her marriage, he says, by buying the house next door. And pets should be banished from the bedroom: ‘Dogs and cats can disturb sleep by yawning, snorting, gasping or moving around. Some patients feel guilty about shutting their pets out of the bedroom, but their sleep can dramatically improve if they do so.’
In my surgery when I need to find out more about a patient’s mental and emotional life it can be enough to ask: ‘How is your sleep?’ People tend to find it easier to talk about sleep than about their mental health, but one segues naturally into the other. Even without sleep, resting calmly in the dark for at least 12 hours a day has been shown to reduce the severity of mania, and can bring an end to episodes of manic psychosis. Patterns of brain activity that support healthy sleep overlap with patterns associated with good mental health.
I have known patients who feel mentally and emotionally robust as long as they’re getting five or six hours of sleep a night; much less and they become tormented by anxiety. I’ve known others with bipolar mood swings for whom sleep is a barometer: when its quality slips they know a manic episode is on the way, and seek help. The derangements of psychosis are often devastating to sleep, but the drugs used to treat psychosis can bring on a somnolence as intolerable as the illness itself.
In the small print of texts on sleep medicine you will often find a reference to a condition called ‘fatal familial insomnia’, so rare that it is largely concentrated within a single family originating in Venice. It is caused by a genetic mutation that leads to the build-up of prions – self-replicating proteins – in the neurons of the brain that are essential for sleep. The disease leads to a progressive intractable insomnia and, eventually, to dementia. In the final weeks, victims’ co-ordination steadily deteriorates and they lose the ability to regulate pulse and temperature; eventually they simply give up breathing. Without sleep, we cannot live.