This ground-breaking book binds together a contemporary understanding of sleep and brain injury, pairing empirical understanding through clinical practice with extensive up-to-date research, to provide a deeply considered approach to these overlapping topics. Firstly, the author discusses the neuroanatomy and architecture of sleep, including the need for sleep, definitions of good sleep, and what can go wrong with sleep. The focus then moves to the neuroanatomical damage and dysfunction from brain injury, and the resultant functional effects. The author then adroitly fuses the two streams of coverage together, focusing on the neurobiological, neurochemical, and functional aspects of both sleep and brain injury to offer new insights as to how they interrelate.
The book then looks towards the applied aspects of treatment and rehabilitation, bringing further thoughts of how, because of this new understanding, we can potentially offer novel treatments for brain injury recovery and sleep problems. In this final practical part, four sleep foundations are given, necessary to optimize the three most common sleep problems and their treatments after brain injury.
This new approach highlights how sleep can affect the specific functional effects of brain injury and how brain injury can exacerbate some of the specific functional effects of sleep problems, thus having the potential to transform the field of neurorehabilitation. It is essential reading for professionals working with brain injury and postgraduate students in clinical neuropsychology.
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This chapter looks at what we know about the basics of sleep. It will introduce the main stages of sleep, highlighting what constitutes each stage. The length, quality, and features of sleep’s fundamental importance to humans will be discussed. Different theories of sleep will be explored, alongside reference to the older pioneers such as Kleitman, followed by Dement, Jouvet, and more modern researchers such as Foster.
As I have previously stated this part of the book will, hopefully, already be understood by those whose primary function is sleep assessment and treatment. It is intended to act as a guide for those working with people who have sustained a brain injury.
We all think we know how sleep works, what it looks like, its benefits, and the harms that accrue if we don’t sleep. I would argue that none of these statements are wholly true.
Sleep appears to be obvious, the person usually lies down, closes their eyes, hears nothing, they begin to relax their mind and their muscles; occasionally they may move, mutter or even fidget. They appear drugged with the water and thus sleep of Lethe. However, from what we now know, as a result of decades of research, in particular during the 20th and current century, it is far from the mythical dulled and relaxing space we once thought. Moreover, a reduction or even excess in essential parts or stages is health limiting and potentially even fatal.
Sleep is an indispensable part of our everyday existence. It makes up approximately one-third of our lives and is as necessary as food and water. A reduction or excess in sleep affects our ability to learn and store memories. It increases the risk of poor mental health, affecting our ability to have a stable mood making us susceptible to a depressed or anxious one. Furthermore, reduced sleep increases morbidity, including well-known diseases of affluence such as diabetes type II, obesity, hypertension, cardiovascular disease, and fatty liver. Indeed, significant reductions eventually lead to death (e.g. numerous, but see Crowther et al., 2021, for a recent review).
As this book will demonstrate sleep is critical for removing toxins and other accumulated waste from the brain and body. It affects every part of the body from immune responses and disease resistance to specific aspects of memory functioning. In recent years the glymphatic system has become more widely understood, the implications of a faulty one are less well documented. Above all it is dynamic, complex, challenging, and as far from the dullness of Lethe as we can imagine.
The rhythm of life
Humans are driven by a number of basic processes like hunger and thirst. Another drive is the Circadian rhythm or sleep-wake cycle. This rhythm is apparent in every living organism, down to very basic ones such as insects. Some of these creatures have polyphasic, some monophasic, and others biphasic sleep patterns.
Quite why using the word creature compels me to think of Margaret Thatcher is unclear. She strongly and rashly disavowed sleep but later suffered Alzheimer’s disease (the link will become very apparent). The truth is no species has evolved to do away with sleep.
Indeed, of all the species studied, the more complex in their evolutionary development, it seems the more complex their need for a particular window of sleep. The parameters within this opportunity for sleep have to operate in a beautifully balanced way for them to be able to work, play, and love well and to the full (probably my only nod to Freud in the entire volume). This applies to humans most of all.
For humans, this rhythm is largely based on the interplay between the brain, body, and the setting and rising of the sun. In that sense, it approximates to 24 hours. I say approximately, as it would be remiss not to mention those pioneers of sleep research Kleitman (see his book Sleep and Wakefulness, 1963) and later Richardson, who spent considerable time underground in a cave to prove that we still have our own endogenous circadian rhythm, but that it is increasingly prolonged and disturbed, without sunlight. One of the most profound aspects of this drive is that it is largely (unless cave bound) propelled by parts of the brain and its connections to the endocrine system. Sleep is thus, a primal part of this fundamental cyclic system, as much as wakefulness is. At a given point, it is not possible to have one without the other. It is well known that each of our individual circadian rhythms is different, this can be a small difference or large. Large differences are demonstrated in “morning larks” and “night owls.” That is the propensity for some of us to appear to get going when others are lagging and vice versa. In other words, we each experience a different chronotypology. Although largely pre-determined by our genes, our understanding of more recent research into both epigenetics and sleep therapy, as we shall see later, suggests this inheritance is far from immutable.
An introductory chemistry set
The circadian rhythm has a number of prominent features and one separate but important parallel contributor to sleep. One of these prominent features controlled largely by the hypothalamus is core body temperature. A balanced core temperature is crucial for internal vital organs, central and peripheral nerve functioning. As with other functions, it has an optimal range under or above which the body finds it more difficult to operate. Depending on the age and the source of this range, for an adult it is approximately between 35.2 and 37.7 degrees Celsius, in other words the range is quite narrow. What we know is the hypothalamus regulates this temperature to increase and decrease at different time points during the day. The outside of the human body, the skin and body parts further away from the central zones of the brain and thoracic regions, has a shell temperature that is in effect, lizard-like. It is dependent on the external temperature in the environment, primarily. We all have a rise in temperature as the day progresses, indeed it is common to reach temperatures, in our core, of 37.8 Celsius (100 degrees Fahrenheit), in the middle of the day when we are at our most active and alert. Now this does of course depend on whether we are larks or owls; each of us has a slightly different middle of the day. The primary reason for stating this is that it is a common myth that the old-fashioned, for those like me long in the tooth, figure of 100 degrees, is a fever. It is also to underscore the narrowness of the range; perhaps only 0.5 more degrees, depending on the scale, would constitute the beginnings of a true fever. During the day we need a relatively higher temperature for working and functioning well.
It is mainly the reverse at night when the core temperature is instructed to lower. A necessary precursor for sleep itself is for the core temperature to fall to its second-lowest point in the circadian rhythm.
The lowest point in core body temperature occurs in the final phases of sleep, usually in the last few hours prior to waking. Given the narrowness of the range discussed, it is startling to note that the core temperature changes by an average of two (2) whole degrees during the course of the early evening through the morning phase of the circadian cycle. Within the sleep stages, non-rapid eye movement (NREM) sleep is the coolest and rapid eye movement (REM) sleep is the hottest. One hypothesis is that the hypothalamus which, as has been shown, is responsible for temperature regulation, needs to rest and recover as well. It largely switches off during REM. What this means is that external temperatures have a more profound effect during REM than at any other point during sleep. This environmental facet will be considered in more depth during a later part of the book. Indeed, as will be shown it is a fundamental part of early treatment in certain types of brain injury.
Another of the prominent structures, of the circadian rhythm, is the suprachiasmatic nucleus (SCN), which I shall discuss in more depth later. Suffice as to note here, it is the biological clock. It is located above the crossover point of the optic nerve and notes repeatedly the amount of light entering each eye for later processing in the occipital lobe. Part of the signalling (post notation) occurs through the hormone melatonin. Soon after the sun is beginning to set, the suprachiasmatic nucleus, in response to the light changes, instructs, via the pineal gland, to release melatonin. This hormone builds up during the evening and provides the setting for us to attempt to sleep. Peak plasma concentration is usually around three to five hours after sunset or darkness occurs. Although, interestingly this peak is much later in certain sleep disorders, such as obstructive sleep apnoea. This partially explains why so many prior to continuous positive airways pressure (CPAP) treatment have become more night owl like, even though they may have started life as larks (see Barnaś et al., 2017; for a wider discussion on its relation with metabolic disease see Song et al., 2019). Melatonin does not generate sleep directly but suggests when the window or sleep opportunity should begin. This increasing concentration peaks later in the evening and as sleep continues (if successful) during the night it begins to reduce.
As the morning light changes and enters the eyelids through to the eyes and then on to the SCN again, it commands the pineal gland to halt its release. In addition, the levels of the hormone cortisol usually rise gradually as we sleep. The night progresses to peak cortisol in the morning, and then as the day continues it gradually diminishes, to be re-set once again during the night’s sleep. Whereas melatonin shows us when the process of sleep should begin, cortisol levels are high in the morning to help us wake, and then diminish to assist sleep by their relative absence at night. This is all part of what has been termed Process C or the circadian clock. In effect Process C sets thresholds for falling asleep and waking up (Daan et al., 1984.)
Process S (the parallel process of sleep and wake) may be said to be the homeostatic process, or sleep propensity (Beersma, 1998.) In this regard, a different chemical, adenosine, begins to have an effect on the system. Whereas melatonin and cortisol may be delineated as both hormones, adenosine is more clearly a neurotransmitter. From first waking, it builds up throughout a day. Peak concentrations of this chemical circulate some 12 to 16 hours after first waking up. At this point, adenosine has stuck to the maximum number of adenosine receptors in the brain which then compel the person to sleep. Adenosine is in its turn driven by the gradual depletion of the body’s glycogen stores. These stores are the powerhouse of our energy. Glycogen utilization is an essential component of the glucose cycle. Without this process growth and other developmental necessities do not occur or at least are problematic, ranging from muscle atrophy through to death (e.g. Peng et al., 2020).
In essence, whilst Process C is almost a relentless clock, analogous to a nuclear one; Process S is mutable, affected by human behaviour (including caffeine intake, Figure 1.1).
Figure1.1 Process C and Process S
However, if both are working in harmony a good sleep-wake cycle would likely occur. I say most likely, as new hormones and neurotransmitters affecting both the sleep and wake cycle are being discovered. One such is the neurotransmitter orexin and its sibling hypocretin. These are not, as was first thought, different names for the same thing. The former refers to protein products, the latter to genetic products; both were not discovered till the late 1990s. Both are intimately linked to food intake and wakefulness. The orexin system, in particular, appears to act as an integrator of metabolic and circadian cycles and processes. One of the central features of orexin is its ability to switch on both lateral aspects of the hypothalamus. This subsequently promotes wakefulness in the brain stem and thence the sensory processing of the thalamus. These discoveries have had a profound effect on our understanding of narcolepsy. At post mortem one of the startling findings in narcoleptic brains was the great, almost total loss of cells that would normally be expected to produce orexin (Mieda and Sakurai, 2016).
The sleep world has four or is that five stages?
Kleitman, once again, was involved in later pioneering research through one of his doctoral students, Aserinsky. In 1952 the latter discovered that infants he was observing appeared to have two kinds of sleep patterns that were repeated during each night. The first involved eye movements and the second did not involve any at all. He along with the former named these two phases non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. Later research by Dement, Kleitman, and Aserinsky found that the brain activity when awake was virtually identical to that found during REM. Moreover, they also seemed to have found a clear link between REM sleep and dreaming. During this period when asleep, the body is almost perfectly still, yet the heart rate will escalate, breathing becomes increasingly shallow, our minds are active (in dreaming and otherwise engaged, e.g. memory work) and of course the eyes move constantly and rapidly.
The other phase (NREM) is subdivided again into at least three and in older understanding four stages. Stages one and two may be described as moderately light sleep and stages three and four are the deepest period of sleep. Stage one is felt through drowsiness and a relaxing of muscle tone. Stage two is considered light sleep; muscle tone is significantly reduced together with a slowing of the heart rate. Stages three and four could be seen as degrees of deep sleep. It is here that the heart slows even further, blood pressure drops, slower brain activity is recorded, muscles are by now fully relaxed, and there is a further decrease in body temperature. Crudely, these stages and their depth are defined by the lack of REM together with the supposed difficulty in rousing a person from them. Thus, stage one has no REM but is potentially the easiest to rouse from (in NREM) but stage four, whilst also without REM is the most difficult to rouse from. These, by now four, stages together with the cycles through the night are known as the architecture of sleep. Today NREM is denoted as N1, N2, and N3, the latter being a subsumed version of the old 3 and 4, and now considered simply deep sleep. It is important to understand that humans have the longest cycle length of any mammal; approximately 90–110 minutes, and that we repeat through the four stages on average five (5) times each night, barring disruptions. It is widely misunderstood that each stage is almost a replication of the last, it isn’t. To begin with the first cycle, although traversing from NREM to REM, dwells in the depths, the second is similarly found submerged in primarily stages three (3) and four (4). Then the transition of cycle three happens in which far more REM sleep is found. Indeed, near to waking the most REM sleep is frequently in evidence. The problem here is, undoubtedly, the descriptors; a muddling can occur between rhythm, cycle, and stage. Suffice to say four stages (one REM and three NREM combined) are repeated to different degrees within five cycles, held captive by the diurnal variation of the circadian rhythm (see the standard sleep graph, known as a hypnogram in Figure 1.2).
Figure1.2 Sleep hypnogram
The other part that needs noting is that all NREM and REM are indispensable for physical and mental well-being. Prolonged deprivation of one or the other will lead to increased morbidity but also ultimately death (numerous, but see Tilley et al., 1992 for a succinct review).
When we say all species, we mean as far as we can demonstrate through behavioural observations of smaller species (bees, beetles, even, molluscs, and so forth) and actual polysomnography results from larger species (e.g. great apes.)
Although common across species, differences emerge between the amounts each needs. It would appear, and it is my contention that there is greater mileage in the theory, that the more complex the nervous system, the more the quantity of sleep is needed. That is to say generally, the degree of concordance breaks down with unusual phyla. Bats have been cited frequently as one outlier, as supposedly needing an inordinately long amount of sleep relative to their size. However, if you glance at some of the litera...
Table of contents
Cover
Half Title
Title Page
Copyright Page
Dedication
Contents
Preface
Foreword
PART I: Sleep
PART II: Brain injury
PART III: The combination of clockwise and counterclockwise vicious cycles
PART IV: Treatments or promoting virtuous cycles
PART V: A recapitulation
References
Index
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