Our lives involve regular, dramatic changes in the degree to which we are aware of our surroundings and our internal states. While awake, we feel alert and aware of the many important things going on around us. Our experiences change dramatically while we are in deep sleep and once again when we are dreaming. Some people also experience altered states of consciousness through meditation, hypnosis, or alcohol and other drugs.
This chapter will discuss states of consciousness with a particular emphasis on sleep. The different stages of sleep will be identified, and sleep disorders will be described. The chapter will close with discussions of altered states of consciousness produced by psychoactive drugs, hypnosis, and meditation.
By the end of this section, you will be able to:
- Understand what is meant by consciousness
- Explain how circadian rhythms are involved in regulating the sleep-wake cycle, and how circadian cycles can be disrupted
- Discuss the concept of sleep debt
We experience different states of consciousness and different levels of awareness on a regular basis. We might even describe consciousness as a continuum that ranges from full awareness to a deep sleep. Sleep is a state marked by relatively low levels of physical activity and reduced sensory awareness that is distinct from periods of rest that occur during wakefulness. Wakefulness is characterized by high levels of sensory awareness, thought, and behavior. Beyond being awake or asleep, there are many other states of consciousness people experience. These include daydreaming, intoxication, and unconsciousness due to anesthesia. We might also experience unconscious states of being via drug-induced anesthesia for medical purposes. Often, we are not completely aware of our surroundings, even when we are fully awake. For instance, have you ever daydreamed while driving home from work or school without really thinking about the drive itself? You were capable of engaging in all of the complex tasks involved with operating a motor vehicle even though you were not aware of doing so. Many of these processes, like much of psychological behavior, are rooted in our biology.
Biological rhythms are internal rhythms of biological activity. A woman’s menstrual cycle is an example of a biological rhythm—a recurring, cyclical pattern of bodily changes. One complete menstrual cycle takes about 28 days—a lunar month—but many biological cycles are much shorter. For example, body temperature fluctuates cyclically over a 24-hour period (Figure 4.2). Alertness is associated with higher body temperatures, and sleepiness with lower body temperatures.
This pattern of temperature fluctuation, which repeats every day, is one example of a circadian rhythm. A circadian rhythm is a biological rhythm that takes place over a period of about 24 hours. Our sleep-wake cycle, which is linked to our environment’s natural light-dark cycle, is perhaps the most obvious example of a circadian rhythm, but we also have daily fluctuations in heart rate, blood pressure, blood sugar, and body temperature. Some circadian rhythms play a role in changes in our state of consciousness.
If we have biological rhythms, then is there some sort of biological clock? In the brain, the hypothalamus, which lies above the pituitary gland, is the main center of homeostasis. Homeostasis is the tendency to maintain a balance, or optimal level, within a biological system.
The brain’s clock mechanism is located in an area of the hypothalamus known as the suprachiasmatic nucleus (SCN). The axons of light-sensitive neurons in the retina provide information to the SCN based on the amount of light present, allowing this internal clock to be synchronized with the outside world (Klein, Moore, & Reppert, 1991; Welsh, Takahashi, & Kay, 2010) (Figure 4.3).
Problems With Circadian Rhythms
Generally, and for most people, our circadian cycles are aligned with the outside world. For example, most people sleep during the night and are awake during the day. One important regulator of sleep-wake cycles is the hormone melatonin. The pineal gland, an endocrine structure located inside the brain that releases melatonin, is thought to be involved in the regulation of various biological rhythms and of the immune system during sleep (Hardeland, Pandi-Perumal, & Cardinali, 2006). Melatonin release is stimulated by darkness and inhibited by light.
There are individual differences in regard to our sleep-wake cycle. For instance, some people would say they are morning people, while others would consider themselves to be night owls. These individual differences in circadian patterns of activity are known as a person’s chronotype, and research demonstrates that morning larks and night owls differ with regard to sleep regulation (Taillard, Philip, Coste, Sagaspe, & Bioulac, 2003). Sleep regulation refers to the brain’s control of switching between sleep and wakefulness as well as coordinating this cycle with the outside world.
Whether lark, owl or somewhere in between, there are situations in which a person’s circadian clock gets out of synchrony with the external environment. One way that this happens involves traveling across multiple time zones. When we do this, we often experience jet lag. Jet lag is a collection of symptoms that results from the mismatch between our internal circadian cycles and our environment. These symptoms include fatigue, sluggishness, irritability, and insomnia (i.e., a consistent difficulty in falling or staying asleep for at least three nights a week over a month’s time) (Roth, 2007).
Individuals who do rotating shift work are also likely to experience disruptions in circadian cycles. Rotating shift work refers to a work schedule that changes from early to late on a daily or weekly basis. For example, a person may work from 7:00 a.m. to 3:00 p.m. on Monday, 3:00 a.m. to 11:00 a.m. on Tuesday, and 11:00 a.m. to 7:00 p.m. on Wednesday. In such instances, the individual’s schedule changes so frequently that it becomes difficult for a normal circadian rhythm to be maintained. This often results in sleeping problems, and it can lead to signs of depression and anxiety. These kinds of schedules are common for individuals working in health care professions and service industries, and they are associated with persistent feelings of exhaustion and agitation that can make someone more prone to making mistakes on the job (Gold et al., 1992; Presser, 1995).
Rotating shift work has pervasive effects on the lives and experiences of individuals engaged in that kind of work, which is clearly illustrated in stories reported in a qualitative study that researched the experiences of middle-aged nurses who worked rotating shifts (West, Boughton & Byrnes, 2009). Several of the nurses interviewed commented that their work schedules affected their relationships with their families. One of the nurses said,
If you’ve had a partner who does work regular job 9 to 5 office hours . . . the ability to spend time, good time with them when you’re not feeling absolutely exhausted . . . that would be one of the problems that I’ve encountered. (West et al., 2009, p. 114)
While disruptions in circadian rhythms can have negative consequences, there are things we can do to help us realign our biological clocks with the external environment. Some of these approaches, such as using a bright light as shown in Figure 4.4, have been shown to alleviate some of the problems experienced by individuals suffering from jet lag or from the consequences of rotating shift work. Because the biological clock is driven by light, exposure to bright light during working shifts and dark exposure when not working can help combat insomnia and symptoms of anxiety and depression (Huang, Tsai, Chen, & Hsu, 2013).
When people have difficulty getting sleep due to their work or the demands of day-to-day life, they accumulate a sleep debt. A person with a sleep debt does not get sufficient sleep on a chronic basis. The consequences of sleep debt include decreased levels of alertness and mental efficiency. Interestingly, since the advent of electric light, the amount of sleep that people get has declined. While we certainly welcome the convenience of having the darkness lit up, we also suffer the consequences of reduced amounts of sleep because we are more active during the nighttime hours than our ancestors were. As a result, many of us sleep less than 7–8 hours a night and accrue a sleep debt. While there is tremendous variation in any given individual’s sleep needs, the National Sleep Foundation (n.d.) cites research to estimate that newborns require the most sleep (between 12 and 18 hours a night) and that this amount declines to just 7–9 hours by the time we are adults.
If you lie down to take a nap and fall asleep very easily, chances are you may have sleep debt. Given that college students are notorious for suffering from significant sleep debt (Hicks, Fernandez, & Pelligrini, 2001; Hicks, Johnson, & Pelligrini, 1992; Miller, Shattuck, & Matsangas, 2010), chances are you and your classmates deal with sleep debt-related issues on a regular basis. In 2015, the National Sleep Foundation updated its sleep duration hours, to better accommodate individual differences. Table 4.1 shows the new recommendations, which describe sleep durations that are “recommended”, “may be appropriate”, and “not recommended”.
|Sleep Needs at Different Ages|
|Age||Recommended||May be appropriate||Not recommended|
|0–3 months||14–17 hours||11–13 hours
|Fewer than 11 hours
More than 19 hours
|4–11 months||12–15 hours||10–11 hours
|Fewer than 10 hours
More than 18 hours
|1–2 years||11–14 hours||9–10 hours
|Fewer than 9 hours
More than 16 hours
|3–5 years||10–13 hours||8–9 hours
|Fewer than 8 hours
More than 14 hours
|6–13 years||9–11 hours||7–8 hours
|Fewer than 7 hours
More than 12 hours
|14–17 years||8–10 hours||7 hours
|Fewer than 7 hours
More than 11 hours
|18–25 years||7–9 hours||6 hours
|Fewer than 6 hours
More than 11 hours
|26–64 years||7–9 hours||6 hours
|Fewer than 6 hours
More than 10 hours
|≥65 years||7–8 hours||5–6 hours
|Fewer than 5 hours
More than 9 hours
Sleep debt and sleep deprivation have significant negative psychological and physiological consequences Figure 4.5. As mentioned earlier, lack of sleep can result in decreased mental alertness and cognitive function. In addition, sleep deprivation often results in depression-like symptoms. These effects can occur as a function of accumulated sleep debt or in response to more acute periods of sleep deprivation. It may surprise you to know that sleep deprivation is associated with obesity, increased blood pressure, increased levels of stress hormones, and reduced immune functioning (Banks & Dinges, 2007). A sleep-deprived individual generally will fall asleep more quickly than if she were not sleep deprived. Some sleep-deprived individuals have difficulty staying awake when they stop moving (for example sitting and watching television or driving a car). That is why individuals suffering from sleep deprivation can also put themselves and others at risk when they put themselves behind the wheel of a car or work with dangerous machinery. Some research suggests that sleep deprivation affects cognitive and motor function as much as, if not more than, alcohol intoxication (Williamson & Feyer, 2000). Research shows that the most severe effects of sleep deprivation occur when a person stays awake for more than 24 hours (Killgore & Weber, 2014; Killgore et al., 2007), or following repeated nights with fewer than four hours in bed (Wickens, Hutchins, Lauk, Seebook, 2015). For example, irritability, distractibility, and impairments in cognitive and moral judgment can occur with fewer than four hours of sleep. If someone stays awake for 48 consecutive hours, they could start to hallucinate.
The amount of sleep we get varies across the lifespan. When we are very young, we spend up to 16 hours a day sleeping. As we grow older, we sleep less. In fact, a meta-analysis, which is a study that combines the results of many related studies, conducted within the last decade indicates that by the time we are 65 years old, we average fewer than 7 hours of sleep per day (Ohayon, Carskadon, Guilleminault, & Vitiello, 2004).
By the end of this section, you will be able to:
- Describe areas of the brain involved in sleep
- Understand hormone secretions associated with sleep
- Describe several theories aimed at explaining the function of sleep
We spend approximately one-third of our lives sleeping. Given the average life expectancy for U.S. citizens falls between 73 and 79 years old (Singh & Siahpush, 2006), we can expect to spend approximately 25 years of our lives sleeping. Some animals never sleep (e.g., some fish and amphibian species); other animals sleep very little without apparent negative consequences (e.g., giraffes); yet some animals (e.g., rats) die after two weeks of sleep deprivation (Siegel, 2008). Why do we devote so much time to sleeping? Is it absolutely essential that we sleep? This section will consider these questions and explore various explanations for why we sleep.
What is Sleep?
You have read that sleep is distinguished by low levels of physical activity and reduced sensory awareness. As discussed by Siegel (2008), a definition of sleep must also include mention of the interplay of the circadian and homeostatic mechanisms that regulate sleep. Homeostatic regulation of sleep is evidenced by sleep rebound following sleep deprivation. Sleep rebound refers to the fact that a sleep-deprived individual will fall asleep more quickly during subsequent opportunities for sleep. Sleep is characterized by certain patterns of activity of the brain that can be visualized using electroencephalography (EEG), and different phases of sleep can be differentiated using EEG as well.
Sleep-wake cycles seem to be controlled by multiple brain areas acting in conjunction with one another. Some of these areas include the thalamus, the hypothalamus, and the pons. As already mentioned, the hypothalamus contains the SCN—the biological clock of the body—in addition to other nuclei that, in conjunction with the thalamus, regulate slow-wave sleep. The pons is important for regulating rapid eye movement (REM) sleep (National Institutes of Health, n.d.).
Sleep is also associated with the secretion and regulation of a number of hormones from several endocrine glands including melatonin, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and growth hormone (National Institutes of Health, n.d.). You have read that the pineal gland releases melatonin during sleep (Figure 4.6). Melatonin is thought to be involved in the regulation of various biological rhythms and the immune system (Hardeland et al., 2006). During sleep, the pituitary gland secretes both FSH and LH which are important in regulating the reproductive system (Christensen et al., 2012; Sofikitis et al., 2008). The pituitary gland also secretes growth hormone, during sleep, which plays a role in physical growth and maturation as well as other metabolic processes (Bartke, Sun, & Longo, 2013).
Why Do We Sleep?
Given the central role that sleep plays in our lives and the number of adverse consequences that have been associated with sleep deprivation, one would think that we would have a clear understanding of why it is that we sleep. Unfortunately, this is not the case; however, several hypotheses have been proposed to explain the function of sleep.
Adaptive Function of Sleep
One popular hypothesis of sleep incorporates the perspective of evolutionary psychology. Evolutionary psychology is a discipline that studies how universal patterns of behavior and cognitive processes have evolved over time as a result of natural selection. Variations and adaptations in cognition and behavior make individuals more or less successful in reproducing and passing their genes to their offspring. One hypothesis from this perspective might argue that sleep is essential to restore resources that are expended during the day. Just as bears hibernate in the winter when resources are scarce, perhaps people sleep at night to reduce their energy expenditures. While this is an intuitive explanation of sleep, there is little research that supports this explanation. In fact, it has been suggested that there is no reason to think that energetic demands could not be addressed with periods of rest and inactivity (Frank, 2006; Rial et al., 2007), and some research has actually found a negative correlation between energetic demands and the amount of time spent sleeping (Capellini, Barton, McNamara, Preston, & Nunn, 2008).
Another evolutionary hypothesis of sleep holds that our sleep patterns evolved as an adaptive response to predatory risks, which increase in darkness. Thus we sleep in safe areas to reduce the chance of harm. Again, this is an intuitive and appealing explanation for why we sleep. Perhaps our ancestors spent extended periods of time asleep to reduce attention to themselves from potential predators. Comparative research indicates, however, that the relationship that exists between predatory risk and sleep is very complex and equivocal. Some research suggests that species that face higher predatory risks sleep fewer hours than other species (Capellini et al., 2008), while other researchers suggest there is no relationship between the amount of time a given species spends in deep sleep and its predation risk (Lesku, Roth, Amlaner, & Lima, 2006).
It is quite possible that sleep serves no single universally adaptive function, and different species have evolved different patterns of sleep in response to their unique evolutionary pressures. While we have discussed the negative outcomes associated with sleep deprivation, it should be pointed out that there are many benefits that are associated with adequate amounts of sleep. A few such benefits listed by the National Sleep Foundation (n.d.) include maintaining a healthy weight, lowering stress levels, improving mood, and increasing motor coordination, as well as a number of benefits related to cognition and memory formation.
Cognitive Function of Sleep
Another theory regarding why we sleep involves sleep’s importance for cognitive function and memory formation (Rattenborg, Lesku, Martinez-Gonzalez, & Lima, 2007). Indeed, we know sleep deprivation results in disruptions in cognition and memory deficits (Brown, 2012), leading to impairments in our abilities to maintain attention, make decisions, and recall long-term memories. Moreover, these impairments become more severe as the amount of sleep deprivation increases (Alhola & Polo-Kantola, 2007). Furthermore, slow-wave sleep after learning a new task can improve resultant performance on that task (Huber, Ghilardi, Massimini, & Tononi, 2004) and seems essential for effective memory formation (Stickgold, 2005). Understanding the impact of sleep on cognitive function should help you understand that cramming all night for a test may be not effective and can even prove counterproductive.
By the end of this section, you will be able to:
- Differentiate between REM and non-REM sleep
- Describe the differences between the three stages of non-REM sleep
- Understand the role that REM and non-REM sleep play in learning and memory
Sleep is not a uniform state of being. Instead, sleep is composed of several different stages that can be differentiated from one another by the patterns of brain wave activity that occur during each stage. These changes in brain wave activity can be visualized using EEG and are distinguished from one another by both the frequency and amplitude of brain waves (Figure 4.7). Sleep can be divided into two different general phases: REM sleep and non-REM (NREM) sleep. Rapid eye movement (REM) sleep is characterized by darting movements of the eyes under closed eyelids. Brain waves during REM sleep appear very similar to brain waves during wakefulness. In contrast, non-REM (NREM) sleep is subdivided into three stages distinguished from each other and from wakefulness by characteristic patterns of brain waves. The first three stages of sleep are NREM sleep, while the fourth and final stage of sleep is REM sleep. In this section, we will discuss each of these stages of sleep and their associated patterns of brain wave activity.
NREM Stages of Sleep
The first stage of NREM sleep is known as stage 1 sleep. Stage 1 sleep is a transitional phase that occurs between wakefulness and sleep, the period during which we drift off to sleep. During this time, there is a slowdown in both the rates of respiration and heartbeat. In addition, stage 1 sleep involves a marked decrease in both overall muscle tension and core body temperature.
In terms of brain wave activity, stage 1 sleep is associated with both alpha and theta waves. The early portion of stage 1 sleep produces alpha waves, which are relatively low frequency (8–13Hz), high amplitude patterns of electrical activity (waves) that become synchronized (Figure 4.8). This pattern of brain wave activity resembles that of someone who is very relaxed, yet awake. As an individual continues through stage 1 sleep, there is an increase in theta wave activity. Theta waves are even lower frequency (4–7 Hz), higher amplitude brain waves than alpha waves. It is relatively easy to wake someone from stage 1 sleep; in fact, people often report that they have not been asleep if they are awoken during stage 1 sleep.
As we move into stage 2 sleep, the body goes into a state of deep relaxation. Theta waves still dominate the activity of the brain, but they are interrupted by brief bursts of activity known as sleep spindles (Figure 4.9). A sleep spindle is a rapid burst of higher frequency brain waves that may be important for learning and memory (Fogel & Smith, 2011; Poe, Walsh, & Bjorness, 2010). In addition, the appearance of K-complexes is often associated with stage 2 sleep. A K-complex is a very high amplitude pattern of brain activity that may in some cases occur in response to environmental stimuli. Thus, K-complexes might serve as a bridge to higher levels of arousal in response to what is going on in our environments (Halász, 1993; Steriade & Amzica, 1998).
Stage 3 is often referred to as deep sleep or slow-wave sleep because this stage is characterized by low frequency (less than 3 Hz), high amplitude delta waves (Figure 4.10). During this time, an individual’s heart rate and respiration slow dramatically. It is much more difficult to awaken someone from sleep during stage 3 than during earlier stages. Interestingly, individuals who have increased levels of alpha brain wave activity (more often associated with wakefulness and transition into stage 1 sleep) during stage 3 often report that they do not feel refreshed upon waking, regardless of how long they slept (Stone, Taylor, McCrae, Kalsekar, & Lichstein, 2008).
As mentioned earlier, REM sleep is marked by rapid movements of the eyes. The brain waves associated with this stage of sleep are very similar to those observed when a person is awake, as shown in Figure 4.11, and this is the period of sleep in which dreaming occurs. It is also associated with paralysis of muscle systems in the body with the exception of those that make circulation and respiration possible. Therefore, no movement of voluntary muscles occurs during REM sleep in a normal individual; REM sleep is often referred to as paradoxical sleep because of this combination of high brain activity and lack of muscle tone. Like NREM sleep, REM has been implicated in various aspects of learning and memory (Wagner, Gais, & Born, 2001; Siegel, 2001).
If people are deprived of REM sleep and then allowed to sleep without disturbance, they will spend more time in REM sleep in what would appear to be an effort to recoup the lost time in REM. This is known as the REM rebound, and it suggests that REM sleep is also homeostatically regulated. Aside from the role that REM sleep may play in processes related to learning and memory, REM sleep may also be involved in emotional processing and regulation. In such instances, REM rebound may actually represent an adaptive response to stress in non-depressed individuals by suppressing the emotional salience of aversive events that occurred in wakefulness (Suchecki, Tiba, & Machado, 2012). Sleep deprivation, in general, is associated with a number of negative consequences (Brown, 2012).
The hypnogram below (Figure 4.12) shows a person’s passage through the stages of sleep.
Dreams and their associated meanings vary across different cultures and periods of time. By the late 19th century, German psychiatrist Sigmund Freud had become convinced that dreams represented an opportunity to gain access to the unconscious. By analyzing dreams, Freud thought people could increase self-awareness and gain valuable insight to help them deal with the problems they faced in their lives. Freud made distinctions between the manifest content and the latent content of dreams. Manifest content is the actual content, or storyline, of a dream. Latent content, on the other hand, refers to the hidden meaning of a dream. For instance, if a woman dreams about being chased by a snake, Freud might have argued that this represents the woman’s fear of sexual intimacy, with the snake serving as a symbol of a man’s penis.
Freud was not the only theorist to focus on the content of dreams. The 20th-century Swiss psychiatrist Carl Jung believed that dreams allowed us to tap into the collective unconscious. The collective unconscious, as described by Jung, is a theoretical repository of information he believed to be shared by everyone. According to Jung, certain symbols in dreams reflected universal archetypes with meanings that are similar for all people regardless of culture or location.
The sleep and dreaming researcher Rosalind Cartwright, however, believes that dreams simply reflect life events that are important to the dreamer. Unlike Freud and Jung, Cartwright’s ideas about dreaming have found empirical support. For example, she and her colleagues published a study in which women going through a divorce were asked several times over a five-month period to report the degree to which their former spouses were on their minds. These same women were awakened during REM sleep in order to provide a detailed account of their dream content. There was a significant positive correlation between the degree to which women thought about their former spouses during waking hours and the number of times their former spouses appeared as characters in their dreams (Cartwright, Agargun, Kirkby, & Friedman, 2006). Recent research (Horikawa, Tamaki, Miyawaki, & Kamitani, 2013) has uncovered new techniques by which researchers may effectively detect and classify the visual images that occur during dreaming by using fMRI for neural measurement of brain activity patterns, opening the way for additional research in this area.
Alan Hobson, a neuroscientist, is credited for developing the activation-synthesis theory of dreaming. Early versions of this theory proposed that dreams were not the meaning-filled representations of angst proposed by Freud and others, but were rather the result of our brain attempting to make sense of (“synthesize”) the neural activity (“activation”) that was happening during REM sleep. Recent adaptations (e.g., Hobson, 2002) continue to update the theory based on accumulating evidence. For example, Hobson (2009) suggests that dreaming may represent a state of protoconsciousness. In other words, dreaming involves constructing a virtual reality in our heads that we might use to help us during wakefulness. Among a variety of neurobiological evidence, John Hobson cites research on lucid dreams as an opportunity to better understand dreaming in general. Lucid dreams are dreams in which certain aspects of wakefulness are maintained during a dream state. In a lucid dream, a person becomes aware of the fact that they are dreaming, and as such, they can control the dream’s content (LaBerge, 1990).
By the end of this section, you will be able to:
- Describe the symptoms and treatments of insomnia
- Recognize the symptoms of several parasomnias
- Describe the symptoms and treatments for sleep apnea
- Recognize risk factors associated with sudden infant death syndrome (SIDS) and steps to prevent it
- Describe the symptoms and treatments for narcolepsy
Many people experience disturbances in their sleep at some point in their lives. Depending on the population and sleep disorder being studied, between 30% and 50% of the population suffers from a sleep disorder at some point in their lives (Bixler, Kales, Soldatos, Kaels, & Healey, 1979; Hossain & Shapiro, 2002; Ohayon, 1997, 2002; Ohayon & Roth, 2002). This section will describe several sleep disorders as well as some of their treatment options.
Insomnia, a consistent difficulty in falling or staying asleep, is the most common of the sleep disorders. Individuals with insomnia often experience long delays between the times that they go to bed and actually fall asleep. In addition, these individuals may wake up several times during the night only to find that they have difficulty getting back to sleep. As mentioned earlier, one of the criteria for insomnia involves experiencing these symptoms for at least three nights a week for at least one month’s time (Roth, 2007).
It is not uncommon for people suffering from insomnia to experience increased levels of anxiety about their inability to fall asleep. This becomes a self-perpetuating cycle because increased anxiety leads to increased arousal, and higher levels of arousal make the prospect of falling asleep even more unlikely. Chronic insomnia is almost always associated with feeling overtired and may be associated with symptoms of depression.
There may be many factors that contribute to insomnia, including age, drug use, exercise, mental status, and bedtime routines. Not surprisingly, insomnia treatment may take one of several different approaches. People who suffer from insomnia might limit their use of stimulant drugs (such as caffeine) or increase their amount of physical exercise during the day. Some people might turn to over-the-counter (OTC) or prescribed sleep medications to help them sleep, but this should be done sparingly because many sleep medications result in dependence and alter the nature of the sleep cycle, and they can increase insomnia over time. Those who continue to have insomnia, particularly if it affects their quality of life, should seek professional treatment.
Some forms of psychotherapy, such as cognitive-behavioral therapy, can help sufferers of insomnia. Cognitive-behavioral therapy is a type of psychotherapy that focuses on cognitive processes and problem behaviors. The treatment of insomnia likely would include stress management techniques and changes in problematic behaviors that could contribute to insomnia (e.g., spending more waking time in bed). Cognitive-behavioral therapy has been demonstrated to be quite effective in treating insomnia (Savard, Simard, Ivers, & Morin, 2005; Williams, Roth, Vatthauer, & McCrae, 2013).
A parasomnia is one of a group of sleep disorders in which unwanted, disruptive motor activity and/or experiences during sleep play a role. Parasomnias can occur in either REM or NREM phases of sleep. Sleepwalking, restless leg syndrome and night terrors are all examples of parasomnias (Mahowald & Schenck, 2000).
In sleepwalking or somnambulism, the sleeper engages in relatively complex behaviors ranging from wandering about to driving an automobile. During periods of sleepwalking, sleepers often have their eyes open, but they are not responsive to attempts to communicate with them. Sleepwalking most often occurs during slow-wave sleep, but it can occur at any time during a sleep period in some affected individuals (Mahowald & Schenck, 2000).
Historically, somnambulism has been treated with a variety of pharmacotherapies ranging from benzodiazepines to antidepressants. However, the success rate of such treatments is questionable. Guilleminault et al. (2005) found that sleepwalking was not alleviated with the use of benzodiazepines. However, all of their somnambulistic patients who also suffered from sleep-related breathing problems showed a marked decrease in sleepwalking when their breathing problems were effectively treated.
REM Sleep Behavior Disorder (RBD)
REM sleep behavior disorder (RBD) occurs when the muscle paralysis associated with the REM sleep phase does not occur. Individuals who suffer from RBD have high levels of physical activity during REM sleep, especially during disturbing dreams. These behaviors vary widely, but they can include kicking, punching, scratching, yelling, and behaving like an animal that has been frightened or attacked. People who suffer from this disorder can injure themselves or their sleeping partners when engaging in these behaviors. Furthermore, these types of behaviors ultimately disrupt sleep, although affected individuals have no memories that these behaviors have occurred (Arnulf, 2012).
This disorder is associated with a number of neurodegenerative diseases such as Parkinson’s disease. In fact, this relationship is so robust that some view the presence of RBD as a potential aid in the diagnosis and treatment of a number of neurodegenerative diseases (Ferini-Strambi, 2011). Clonazepam, an anti-anxiety medication with sedative properties, is most often used to treat RBD. It is administered alone or in conjunction with doses of melatonin (the hormone secreted by the pineal gland). As part of treatment, the sleeping environment is often modified to make it a safer place for those suffering from RBD (Zangini, Calandra-Buonaura, Grimaldi, & Cortelli, 2011).
A person with restless leg syndrome has uncomfortable sensations in the legs during periods of inactivity or when trying to fall asleep. This discomfort is relieved by deliberately moving the legs, which, not surprisingly, contributes to difficulty in falling or staying asleep. Restless leg syndrome is quite common and has been associated with a number of other medical diagnoses, such as chronic kidney disease and diabetes (Mahowald & Schenck, 2000). There are a variety of drugs that treat restless leg syndrome: benzodiazepines, opiates, and anticonvulsants (Restless Legs Syndrome Foundation, n.d.).
Night terrors result in a sense of panic in the sufferer and are often accompanied by screams and attempts to escape from the immediate environment (Mahowald & Schenck, 2000). Although individuals suffering from night terrors appear to be awake, they generally have no memories of the events that occurred, and attempts to console them are ineffective. Typically, individuals suffering from night terrors will fall back asleep again within a short time. Night terrors apparently occur during the NREM phase of sleep (Provini, Tinuper, Bisulli, & Lagaresi, 2011). Generally, treatment for night terrors is unnecessary unless there is some underlying medical or psychological condition that is contributing to the night terrors (Mayo Clinic, n.d.).
Sleep apnea is defined by episodes during which a sleeper’s breathing stops. These episodes can last 10–20 seconds or longer and often are associated with brief periods of arousal. While individuals suffering from sleep apnea may not be aware of these repeated disruptions in sleep, they do experience increased levels of fatigue. Many individuals diagnosed with sleep apnea first seek treatment because their sleeping partners indicate that they snore loudly and/or stop breathing for extended periods of time while sleeping (Henry & Rosenthal, 2013). Sleep apnea is much more common in overweight people and is often associated with loud snoring. Surprisingly, sleep apnea may exacerbate cardiovascular disease (Sánchez-de-la-Torre, Campos-Rodriguez, & Barbé, 2012). While sleep apnea is less common in thin people, anyone, regardless of their weight, who snores loudly or gasps for air while sleeping, should be checked for sleep apnea.
While people are often unaware of their sleep apnea, they are keenly aware of some of the adverse consequences of insufficient sleep. Consider a patient who believed that as a result of his sleep apnea he “had three car accidents in six weeks. They were ALL my fault. Two of them I didn’t even know I was involved in until afterward” (Henry & Rosenthal, 2013, p. 52). It is not uncommon for people suffering from undiagnosed or untreated sleep apnea to fear that their careers will be affected by the lack of sleep, illustrated by this statement from another patient, “I’m in a job where there’s a premium on being mentally alert. I was really sleepy… and having trouble concentrating…. It was getting to the point where it was kind of scary” (Henry & Rosenthal, 2013, p. 52).
There are two types of sleep apnea: obstructive sleep apnea and central sleep apnea. Obstructive sleep apnea occurs when an individual’s airway becomes blocked during sleep, and the air is prevented from entering the lungs. In central sleep apnea, disruption in signals sent from the brain that regulate breathing cause periods of interrupted breathing (White, 2005).
One of the most common treatments for sleep apnea involves the use of a special device during sleep. A continuous positive airway pressure (CPAP) device includes a mask that fits over the sleeper’s nose and mouth, which is connected to a pump that pumps air into the person’s airways, forcing them to remain open, as shown in Figure 4.13. Some newer CPAP masks are smaller and cover only the nose. This treatment option has proven to be effective for people suffering from mild to severe cases of sleep apnea (McDaid et al., 2009). However, alternative treatment options are being explored because consistent compliance by users of CPAP devices is a problem. Recently, a new EPAP (expiratory positive air pressure) device has shown promise in double-blind trials as one such alternative (Berry, Kryger, & Massie, 2011).
In sudden infant death syndrome (SIDS) an infant stops breathing during sleep and dies. Infants younger than 12 months appear to be at the highest risk for SIDS, and boys have a greater risk than girls. A number of risk factors have been associated with SIDS including premature birth, smoking within the home, and hyperthermia. There may also be differences in both brain structure and function in infants that die from SIDS (Berkowitz, 2012; Mage & Donner, 2006; Thach, 2005).
The substantial amount of research on SIDS has led to a number of recommendations to parents to protect their children (Figure 4.14). For one, research suggests that infants should be placed on their backs when put down to sleep, and their cribs should not contain any items which pose suffocation threats, such as blankets, pillows, or padded crib bumpers (cushions that cover the bars of a crib). Infants should not have caps placed on their heads when put down to sleep in order to prevent overheating, and people in the child’s household should abstain from smoking in the home. Recommendations like these have helped to decrease the number of infant deaths from SIDS in recent years (Mitchell, 2009; Task Force on Sudden Infant Death Syndrome, 2011).
Unlike the other sleep disorders described in this section, a person with narcolepsy cannot resist falling asleep at inopportune times. These sleep episodes are often associated with cataplexy, which is a lack of muscle tone or muscle weakness, and in some cases involves complete paralysis of the voluntary muscles. This is similar to the kind of paralysis experienced by healthy individuals during REM sleep (Burgess & Scammell, 2012; Hishikawa & Shimizu, 1995; Luppi et al., 2011). Narcoleptic episodes take on other features of REM sleep. For example, around one-third of individuals diagnosed with narcolepsy experience vivid, dream-like hallucinations during narcoleptic attacks (Chokroverty, 2010).
Surprisingly, narcoleptic episodes are often triggered by states of heightened arousal or stress. The typical episode can last from a minute or two to half an hour. Once awakened from a narcoleptic attack, people report that they feel refreshed (Chokroverty, 2010). Obviously, regular narcoleptic episodes could interfere with the ability to perform one’s job or complete schoolwork, and in some situations, narcolepsy can result in significant harm and injury (e.g., driving a car or operating machinery or other potentially dangerous equipment).
Generally, narcolepsy is treated using psychomotor stimulant drugs, such as amphetamines (Mignot, 2012). These drugs promote increased levels of neural activity. Narcolepsy is associated with reduced levels of the signaling molecule hypocretin in some areas of the brain (De la Herrán-Arita & Drucker-Colín, 2012; Han, 2012), and the traditional stimulant drugs do not have direct effects on this system. Therefore, it is quite likely that new medications that are developed to treat narcolepsy will be designed to target the hypocretin system.
There is a tremendous amount of variability among sufferers, both in terms of how symptoms of narcolepsy manifest and the effectiveness of currently available treatment options. This is illustrated by McCarty’s (2010) case study of a 50-year-old woman who sought help for the excessive sleepiness during normal waking hours that she had experienced for several years. She indicated that she had fallen asleep at inappropriate or dangerous times, including while eating, while socializing with friends, and while driving her car. During periods of emotional arousal, the woman complained that she felt some weakness on the right side of her body. Although she did not experience any dream-like hallucinations, she was diagnosed with narcolepsy as a result of sleep testing. In her case, the fact that her cataplexy was confined to the right side of her body was quite unusual. Early attempts to treat her condition with a stimulant drug alone were unsuccessful. However, when a stimulant drug was used in conjunction with a popular antidepressant, her condition improved dramatically.
By the end of this section, you will be able to:
- Describe the diagnostic criteria for substance use disorders
- Identify the neurotransmitter systems impacted by various categories of drugs
- Describe how different categories of drugs affect behavior and experience
While we all experience altered states of consciousness in the form of sleep on a regular basis, some people use drugs and other substances that result in altered states of consciousness as well. This section will present information relating to the use of various psychoactive drugs and problems associated with such use. This will be followed by brief descriptions of the effects of some of the more well-known drugs commonly used today.
Substance Use Disorders
The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) is used by clinicians to diagnose individuals suffering from various psychological disorders. Drug use disorders are addictive disorders, and the criteria for specific substance (drug) use disorders are described in DSM-5. A person who has a substance use disorder often uses more of the substance than they originally intended to and continues to use that substance despite experiencing significant adverse consequences. In individuals diagnosed with a substance use disorder, there is a compulsive pattern of drug use that is often associated with both physical and psychological dependence.
Physical dependence involves changes in normal bodily functions—the user will experience withdrawal from the drug upon cessation of use. In contrast, a person who has psychological dependence has an emotional, rather than physical, need for the drug and may use the drug to relieve psychological distress. Tolerance is linked to physiological dependence, and it occurs when a person requires more and more drug to achieve effects previously experienced at lower doses. Tolerance can cause the user to increase the amount of drug used to a dangerous level—even to the point of overdose and death.
Drug withdrawal includes a variety of negative symptoms experienced when drug use is discontinued. These symptoms usually are the opposite of the effects of the drug. For example, withdrawal from sedative drugs often produces unpleasant arousal and agitation. In addition to withdrawal, many individuals who are diagnosed with substance use disorders will also develop tolerance to these substances. Psychological dependence, or drug craving, is a recent addition to the diagnostic criteria for substance use disorder in DSM-5. This is an important factor because we can develop tolerance and experience withdrawal from any number of drugs that we do not abuse. In other words, physical dependence in and of itself is of limited utility in determining whether or not someone has a substance use disorder.
The effects of all psychoactive drugs occur through their interactions with our endogenous neurotransmitter systems. Many of these drugs, and their relationships, are shown in Table 4.2. As you have learned, drugs can act as agonists or antagonists of a given neurotransmitter system. An agonist facilitates the activity of a neurotransmitter system, and antagonists impede neurotransmitter activity.
|Drugs and Their Effects|
|Class of Drug||Examples||Effects on the Body||Effects When Used||Psychologically Addicting?|
|Stimulants||Cocaine, amphetamines (including some ADHD medications such as Adderall), methamphetamines, MDMA (“Ecstasy” or “Molly”)||Increased heart rate, blood pressure, body temperature||Increased alertness, mild euphoria, decreased appetite in low doses. High doses increase agitation, paranoia, can cause hallucinations. Some can cause heightened sensitivity to physical stimuli. High doses of MDMA can cause brain toxicity and death.||Yes|
|Sedative-Hypnotics (“Depressants”)||Alcohol, barbiturates (e.g., secobarbital, pentobarbital), Benzodiazepines (e.g., Xanax)||Decreased heart rate, blood pressure||Low doses increase relaxation, decrease inhibitions. High doses can induce sleep, cause motor disturbance, memory loss, decreased respiratory function, and death.||Yes|
|Opiates||Opium, Heroin, Fentanyl, Morphine, Oxycodone, Vicoden, methadone, and other prescription pain relievers||Decreased pain, pupil dilation, decreased gut motility, decreased respiratory function||Pain relief, euphoria, sleepiness. High doses can cause death due to respiratory depression.||Yes|
|Hallucinogens||Marijuana, LSD, Peyote, mescaline, DMT, dissociative anesthetics including ketamine and PCP||Increased heart rate and blood pressure that may dissipate over time||Mild to intense perceptual changes with high variability in effects based on strain, method of ingestion, and individual differences||Yes|
Alcohol and Other Depressants
Ethanol, which we commonly refer to as alcohol, is in a class of psychoactive drugs known as depressants (Figure 4.15). A depressant is a drug that tends to suppress central nervous system activity. Other depressants include barbiturates and benzodiazepines. These drugs share in common their ability to serve as agonists of the gamma-Aminobutyric acid (GABA) neurotransmitter system. Because GABA has a quieting effect on the brain, GABA agonists also have a quieting effect; these types of drugs are often prescribed to treat both anxiety and insomnia.
Acute alcohol administration results in a variety of changes to consciousness. At rather low doses, alcohol use is associated with feelings of euphoria. As the dose increases, people report feeling sedated. Generally, alcohol is associated with decreases in reaction time and visual acuity lowered levels of alertness, and reduction in behavioral control. With excessive alcohol use, a person might experience a complete loss of consciousness and/or difficulty remembering events that occurred during a period of intoxication (McKim & Hancock, 2013). In addition, if a pregnant woman consumes alcohol, her infant may be born with a cluster of birth defects and symptoms collectively called fetal alcohol spectrum disorder (FASD) or fetal alcohol syndrome (FAS).
With repeated use of many central nervous system depressants, such as alcohol, a person becomes physically dependent upon the substance and will exhibit signs of both tolerance and withdrawal. Psychological dependence on these drugs is also possible. Therefore, the abuse potential of central nervous system depressants is relatively high.
Drug withdrawal is usually an aversive experience, and it can be a life-threatening process in individuals who have a long history of very high doses of alcohol and/or barbiturates. This is of such concern that people who are trying to overcome addiction to these substances should only do so under medical supervision.
Stimulants are drugs that tend to increase overall levels of neural activity. Many of these drugs act as agonists of the dopamine neurotransmitter system. Dopamine activity is often associated with reward and craving; therefore, drugs that affect dopamine neurotransmission often have abuse liability. Drugs in this category include cocaine, amphetamines (including methamphetamine), cathinones (i.e., bath salts), MDMA (ecstasy), nicotine, and caffeine.
Cocaine can be taken in multiple ways. While many users snort cocaine, intravenous injection and inhalation (smoking) are also common. The freebase version of cocaine, known as crack, is a potent, smokable version of the drug. Like many other stimulants, cocaine agonizes the dopamine neurotransmitter system by blocking the reuptake of dopamine in the neuronal synapse.
In recent years, methamphetamine (meth) use has become increasingly widespread. Methamphetamine is a type of amphetamine that can be made from ingredients that are readily available (e.g., medications containing pseudoephedrine, a compound found in many over-the-counter cold and flu remedies). Despite recent changes in laws designed to make obtaining pseudoephedrine more difficult, methamphetamine continues to be an easily accessible and relatively inexpensive drug option (Shukla, Crump, & Chrisco, 2012).
Stimulant users seek a euphoric high, feelings of intense elation and pleasure, especially in those users who take the drug via intravenous injection or smoking. MDMA (3.4-methelynedioxy-methamphetamine, commonly known as “ecstasy” or “Molly”) is a mild stimulant with perception-altering effects. It is typically consumed in pill form. Users experience increased energy, feelings of pleasure, and emotional warmth. Repeated use of these stimulants can have significant adverse consequences. Users can experience physical symptoms that include nausea, elevated blood pressure, and increased heart rate. In addition, these drugs can cause feelings of anxiety, hallucinations, and paranoia (Fiorentini et al., 2011). Normal brain functioning is altered after repeated use of these drugs. For example, repeated use can lead to overall depletion among the monoamine neurotransmitters (dopamine, norepinephrine, and serotonin). The depletion of certain neurotransmitters can lead to mood dysphoria, cognitive problems, and other factors. This can lead to people compulsively using stimulants such as cocaine and amphetamines, in part to try to re-establish the person’s physical and psychological pre-use baseline. (Jayanthi & Ramamoorthy, 2005; Rothman, Blough, & Baumann, 2007).
Caffeine is another stimulant drug. While it is probably the most commonly used drug in the world, the potency of this particular drug pales in comparison to the other stimulant drugs described in this section. Generally, people use caffeine to maintain increased levels of alertness and arousal. Caffeine is found in many common medicines (such as weight loss drugs), beverages, foods, and even cosmetics (Herman & Herman, 2013). While caffeine may have some indirect effects on dopamine neurotransmission, its primary mechanism of action involves antagonizing adenosine activity (Porkka-Heiskanen, 2011). Adenosine is a neurotransmitter that promotes sleep. Caffeine is an adenosine antagonist, so caffeine inhibits the adenosine receptors, thus decreasing sleepiness and promoting wakefulness.
While caffeine is generally considered a relatively safe drug, high blood levels of caffeine can result in insomnia, agitation, muscle twitching, nausea, irregular heartbeat, and even death (Reissig, Strain, & Griffiths, 2009; Wolt, Ganetsky, & Babu, 2012). In 2012, Kromann and Nielson reported on a case study of a 40-year-old woman who suffered significant ill effects from her use of caffeine. The woman used caffeine in the past to boost her mood and to provide energy, but over the course of several years, she increased her caffeine consumption to the point that she was consuming three liters of soda each day. Although she had been taking a prescription antidepressant, her symptoms of depression continued to worsen and she began to suffer physically, displaying significant warning signs of cardiovascular disease and diabetes. Upon admission to an outpatient clinic for treatment of mood disorders, she met all of the diagnostic criteria for substance dependence and was advised to dramatically limit her caffeine intake. Once she was able to limit her use to less than 12 ounces of soda a day, both her mental and physical health gradually improved. Despite the prevalence of caffeine use and the large number of people who confess to suffering from caffeine addiction, this was the first published description of soda dependence appearing in the scientific literature.
Nicotine is highly addictive, and the use of tobacco products is associated with increased risks of heart disease, stroke, and a variety of cancers. Nicotine exerts its effects through its interaction with acetylcholine receptors. Acetylcholine functions as a neurotransmitter in motor neurons. In the central nervous system, it plays a role in arousal and reward mechanisms. Nicotine is most commonly used in the form of tobacco products like cigarettes or chewing tobacco; therefore, there is a tremendous interest in developing effective smoking cessation techniques. To date, people have used a variety of nicotine replacement therapies in addition to various psychotherapeutic options in an attempt to discontinue their use of tobacco products. In general, smoking cessation programs may be effective in the short term, but it is unclear whether these effects persist (Cropley, Theadom, Pravettoni, & Webb, 2008; Levitt, Shaw, Wong, & Kaczorowski, 2007; Smedslund, Fisher, Boles, & Lichtenstein, 2004). Vaping as a means to deliver nicotine is becoming increasingly popular, especially among teens and young adults. Vaping uses battery-powered devices, sometimes called e-cigarettes, that deliver liquid nicotine and flavorings as a vapor. Originally reported as a safe alternative to the known cancer-causing agents found in cigarettes, vaping is now known to be very dangerous and has led to serious lung disease and death in users.
An opioid is one of a category of drugs that includes heroin, morphine, methadone, and codeine. Opioids have analgesic properties; that is, they decrease pain. Humans have an endogenous opioid neurotransmitter system—the body makes small quantities of opioid compounds that bind to opioid receptors reducing pain and producing euphoria. Thus, opioid drugs, which mimic this endogenous painkilling mechanism, have an extremely high potential for abuse. Natural opioids, called opiates, are derivatives of opium, which is a naturally occurring compound found in the poppy plant. There are now several synthetic versions of opiate drugs (correctly called opioids) that have very potent painkilling effects, and they are often abused. For example, the National Institutes of Drug Abuse has sponsored research that suggests the misuse and abuse of the prescription pain killers hydrocodone and oxycodone are significant public health concerns (Maxwell, 2006). In 2013, the U.S. Food and Drug Administration recommended tighter controls on their medical use.
Historically, heroin has been a major opioid drug of abuse (Figure 4.17). Heroin can be snorted, smoked, or injected intravenously. Heroin produces intense feelings of euphoria and pleasure, which are amplified when the heroin is injected intravenously. Following the initial “rush,” users experience 4–6 hours of “going on the nod,” alternating between conscious and semi-conscious states. Heroin users often shoot the drug directly into their veins. Some people who have injected many times into their arms will show “track marks,” while other users will inject into areas between their fingers or between their toes, so as not to show obvious track marks and, like all abusers of intravenous drugs, have an increased risk for contraction of both tuberculosis and HIV.
Aside from their utility as analgesic drugs, opioid-like compounds are often found in cough suppressants, anti-nausea, and anti-diarrhea medications. Given that withdrawal from a drug often involves an experience opposite to the effect of the drug, it should be no surprise that opioid withdrawal resembles a severe case of the flu. While opioid withdrawal can be extremely unpleasant, it is not life-threatening (Julien, 2005). Still, people experiencing opioid withdrawal may be given methadone to make the withdrawal from the drug less difficult. Methadone is a synthetic opioid that is less euphorigenic than heroin and similar drugs. Methadone clinics help people who previously struggled with opioid addiction manage withdrawal symptoms through the use of methadone. Other drugs, including the opioid buprenorphine, have also been used to alleviate symptoms of opiate withdrawal.
Codeine is an opioid with relatively low potency. It is often prescribed for minor pain, and it is available over-the-counter in some other countries. Like all opioids, codeine does have abuse potential. In fact, abuse of prescription opioid medications is becoming a major concern worldwide (Aquina, Marques-Baptista, Bridgeman, & Merlin, 2009; Casati, Sedefov, & Pfeiffer-Gerschel, 2012).
A hallucinogen is one of a class of drugs that results in profound alterations in sensory and perceptual experiences (Figure 4.18). In some cases, users experience vivid visual hallucinations. It is also common for these types of drugs to cause hallucinations of body sensations (e.g., feeling as if you are a giant) and a skewed perception of the passage of time.
As a group, hallucinogens are incredibly varied in terms of the neurotransmitter systems they affect. Mescaline and LSD are serotonin agonists, and PCP (angel dust) and ketamine (an animal anesthetic) act as antagonists of the NMDA glutamate receptor. In general, these drugs are not thought to possess the same sort of abuse potential as other classes of drugs discussed in this section.
While medical marijuana laws have been passed on a state-by-state basis, federal laws still classify this as an illicit substance, making conducting research on the potentially beneficial medicinal uses of marijuana problematic. There is quite a bit of controversy within the scientific community as to the extent to which marijuana might have medicinal benefits due to a lack of large-scale, controlled research (Bostwick, 2012). As a result, many scientists have urged the federal government to allow for the relaxation of current marijuana laws and classifications in order to facilitate a more widespread study of the drug’s effects (Aggarwal et al., 2009; Bostwick, 2012; Kogan & Mechoulam, 2007).
Until recently, the United States Department of Justice routinely arrested people involved and seized marijuana used in medicinal settings. In the latter part of 2013, however, the United States Department of Justice issued statements indicating that they would not continue to challenge state medical marijuana laws. This shift in policy may be in response to the scientific community’s recommendations and/or reflect changing public opinion regarding marijuana.
By the end of this section, you will be able to:
- Define hypnosis and meditation
- Understand the similarities and differences between hypnosis and meditation
Our states of consciousness change as we move from wakefulness to sleep. We also alter our consciousness through the use of various psychoactive drugs. This final section will consider hypnotic and meditative states as additional examples of altered states of consciousness experienced by some individuals.
Hypnosis is a state of extreme self-focus and attention in which minimal attention is given to external stimuli. In the therapeutic setting, a clinician may use relaxation and suggestion in an attempt to alter the thoughts and perceptions of a patient. Hypnosis has also been used to draw out information believed to be buried deeply in someone’s memory. For individuals who are especially open to the power of suggestion, hypnosis can prove to be a very effective technique, and brain imaging studies have demonstrated that hypnotic states are associated with global changes in brain functioning (Del Casale et al., 2012; Guldenmund, Vanhaudenhuyse, Boly, Laureys, & Soddu, 2012).
Historically, hypnosis has been viewed with some suspicion because of its portrayal in popular media and entertainment (Figure 4.20). Therefore, it is important to make a distinction between hypnosis as an empirically based therapeutic approach versus as a form of entertainment. Contrary to popular belief, individuals undergoing hypnosis usually have clear memories of the hypnotic experience and are in control of their own behaviors. While hypnosis may be useful in enhancing memory or a skill, such enhancements are very modest in nature (Raz, 2011).
How exactly does a hypnotist bring a participant to a state of hypnosis? While there are variations, there are four parts that appear consistent in bringing people into the state of suggestibility associated with hypnosis (National Research Council, 1994). These components include:
- The participant is guided to focus on one thing, such as the hypnotist’s words or a ticking watch.
- The participant is made comfortable and is directed to be relaxed and sleepy.
- The participant is told to be open to the process of hypnosis, trust the hypnotist, and let go.
- The participant is encouraged to use his or her imagination.
These steps are conducive to being open to the heightened suggestibility of hypnosis.
People vary in terms of their ability to be hypnotized, but a review of available research suggests that most people are at least moderately hypnotizable (Kihlstrom, 2013). Hypnosis in conjunction with other techniques is used for a variety of therapeutic purposes and has shown to be at least somewhat effective for pain management, treatment of depression and anxiety, smoking cessation, and weight loss (Alladin, 2012; Elkins, Johnson, & Fisher, 2012; Golden, 2012; Montgomery, Schnur, & Kravits, 2012).
How does hypnosis work? Two theories attempt to answer this question: One theory views hypnosis as dissociation and the other theory views it as the performance of a social role. According to the dissociation view, hypnosis is effectively a dissociated state of consciousness, much like our earlier example where you may drive to work, but you are only minimally aware of the process of driving because your attention is focused elsewhere. This theory is supported by Ernest Hilgard’s research into hypnosis and pain. In Hilgard’s experiments, he induced participants into a state of hypnosis and placed their arms into ice water. Participants were told they would not feel pain, but they could press a button if they did; while they reported not feeling pain, they did, in fact, press the button, suggesting a dissociation of consciousness while in the hypnotic state (Hilgard & Hilgard, 1994).
Taking a different approach to explain hypnosis, the social-cognitive theory of hypnosis sees people in hypnotic states as performing the social role of a hypnotized person. As you will learn when you study social roles, people’s behavior can be shaped by their expectations of how they should act in a given situation. Some view a hypnotized person’s behavior not as an altered or dissociated state of consciousness, but as their fulfillment of the social expectations for that role (Coe, 2009; Coe & Sarbin, 1966).
Meditation is the act of focusing on a single target (such as the breath or a repeated sound) to increase awareness of the moment. While hypnosis is generally achieved through the interaction of a therapist and the person being treated, an individual can perform meditation alone. Often, however, people wishing to learn to meditate receive some training in techniques to achieve a meditative state.
Although there are a number of different techniques in use, the central feature of all meditation is clearing the mind in order to achieve a state of relaxed awareness and focus (Chen et al., 2013; Lang et al., 2012). Mindfulness meditation has recently become popular. In the variation of mindful meditation, the meditator’s attention is focused on some internal process or an external object (Zeidan, Grant, Brown, McHaffie, & Coghill, 2012).
Meditative techniques have their roots in religious practices (Figure 4.21), but their use has grown in popularity among practitioners of alternative medicine. Research indicates that meditation may help reduce blood pressure, and the American Heart Association suggests that meditation might be used in conjunction with more traditional treatments as a way to manage hypertension, although there is not sufficient data for a recommendation to be made (Brook et al., 2013). Like hypnosis, meditation also shows promise in stress management, sleep quality (Caldwell, Harrison, Adams, Quin, & Greeson, 2010), treatment of mood and anxiety disorders (Chen et al., 2013; Freeman et al., 2010; Vøllestad, Nielsen, & Nielsen, 2012), and pain management (Reiner, Tibi, & Lipsitz, 2013).