Sleep and Consciousness

Sleep and Dreaming

The fact that species with higher metabolic rates typically spend more time in sleep supports the hypothesis that sleep is restorative.

Support for this idea comes from the observation that species with higher metabolic rates typically spend more time in sleep.

A less obvious explanation is the adaptive hypothesis.

According to this view, the amount of sleep an animal engages in depends on the availability of food and on safety considerations.

      A circadian rhythm is a rhythm that is about a day in length.

The main biological clock that controls these rhythms in mammals is the suprachiasmatic nucleus (SCN) of the hypothalamus.

Lesioning the SCN in rats abolishes the normal 24-hour rhythms of sleep, activity, body temperature, drinking, and steroid secretion.

The SCN is entrained to the solar day by cues called zeitgebers (“time-givers”).

The SCN regulates the pineal gland’s secretion of melatonin, a hormone that induces sleepiness.

Melatonin is often used to combat jet lag and to treat insomnia in shift workers and in the blind.

Light resets the biological clock by suppressing melatonin secretion.

Light information reaches the SCN by way of a direct connection from the retinas called the retinohypothalamic pathway.

Ganglion cells in the retina contain melanopsin, which is a light-sensitive substance, or photopigment.

The melanopsin is located in widely branching dendrites, which suits the cells for detecting the overall level of light, as opposed to contributing to image formation.

Riding on the day-long wave of the circadian rhythm are several ultradian rhythms, rhythms that are shorter than a day in length.

Hormone production, urinary output, alertness, and other functions follow regular cycles throughout the day.

The most important measure of sleep activity is the electroencephalogram, or EEG.

When a person is awake, the EEG is a mix of alpha and beta waves.

As the person slips into the light first stage of sleep, the EEG shifts to theta waves.

About 10 minutes later Stage 2 begins, indicated by:

Sleep spindles, brief bursts of 12- to 14-Hz waves;

K complexes, sharp, large waves that occur once a minute.

Stage 3 and 4 are known as slow wave sleep and are characterized by large, slow delta waves at a frequency of 1-3 Hz

After stage 4 the sleeper moves rather quickly back through the stages in reverse order.

But rather than returning to Stage 1, the sleeper enters REM sleep.

REM, or rapid eye movement, sleep is so called because the eyes dart back and forth horizontally during this stage.

     According to the activation-synthesis hypothesis, during  REM                 sleep  the  forebrain integrates neural activity generated by the brain stem with information stored in memory.

In other words, the brain uses information from memory to impose meaning on nonsensical random input.

One biological hypothesis is that REM sleep promotes neural development during childhood.

According to this hypothesis, excitation that spreads through the brain from the pons during REM sleep encourages differentiation, maturation, and myelination in higher brain centers.

Early ideas about non-REM functions focused on rest and restoration, inspired by studies showing that slow wave sleep increases following exercise.

However, this effect appears to be due to overheating rather than fatigue.

Horne (1988) believes that slow wave sleep is more related to the increase in the temperature of the brain than the increase in body temperature.

According to Horne (1992), slow wave sleep promotes cerebral recovery, especially in the prefrontal cortex.

The amount of REM increases during the sleep period following learning, and REM deprivation after learning reduces retention.

There is increasing evidence from both animal and human studies that non-REM sleep is also important for learning.

A study indicated that consolidation is a multi-step process requiring a combination of REM and slow wave sleep.

According to Ribeiro and his colleagues (2004), neuronal replay is strongest during non-REM sleep and represents recall and amplification of the hippocampal activity that occurred during learning.

Then during REM sleep the hippocampus upregulates genes in the cortex that are involved in synaptic plasticity, implementing the transfer of memory from hippocampus to cortex.

According to Crick and Mitchison’s (1995) reverse learning hypothesis, REM is also a period of memory erasure.

They suggest that neural networks involved in memory must have a way to purge purge themselves of erroneous connections; this hypothesis is supported by: enhanced performance of computer neural networks with reverse learning, and the fact that mammals without REM sleep have large brains for their body size.

Sleep is homeostatic, in that a period of deprivation is followed by a lengthened sleep period.

Adenosine provides at least one of the mechanisms of sleep homeostasis.

During wakefulness adenosine accumulates in the basal forebrain area.

It inhibits arousal-producing neurons there, inducing drowsiness and reducing EEG activation.

Another location where adenosine increases sleep is the preoptic area of the hypothalamus.

Warming this part of the hypothalamus activates sleep-related cells, inhibits waking-related cells in the basal forebrain, and enhances slow-wave EEG.

Neurons in part of the preoptic area, the ventrolateral preoptic nucleus, double their rate of firing during sleep, and inhibit neurons in arousal areas.

      The arousal system consists of two major pathways.

Neurons from the PPT/LDT activate areas crucial for transmission to the cortex and desynchronize the EEG; they are also active during REM sleep.

The second pathway activates the cortex to facilitate the processing of inputs from the thalamus.

The arousing pathway is completed by neurons from the lateral hypothalamus.

Lateral hypothalamus neurons that release hypocretin are most active during waking, while those that release melanocortin-concentrating hormone are active during REM sleep.

The pons is the source of PGO waves seen during REM sleep.

Arousal by PGO waves may account for the EEG desynchrony and the visual imagery of REM sleep.

     Insomnia is the inability to sleep or to obtain adequate quality sleep, 

    to  the extent that the person feels inadequately rested.

Insomnia can be brought on by a number of factors, such as stress.

Insolmnia also occurs frequently in people with psychological problems, especially affective disorders.

Some of the sleep disorders are related to specific sleep stages.

Bedwetting, night terrors, and sleep walking occur during slow wave sleep.

Although sleepwalking is most frequent in childhood, about three to eight percent of adults sleepwalk.

Sleepwalking is at least partially genetic, and can be triggered by stress, alcohol, and sleep deprivation.

Narcolepsy is a disorder in which individuals fall asleep suddenly during the daytime and go directly into REM sleep.

Another symptom of narcolepsy is cataplexy, in which the person has a sudden experience of one component of REM sleep – atonia – and falls to the floor paralyzed but fully awake.

In REM sleep behavior disorder individuals are uncharacteristically physically active during REM sleep, often to the point of injuring themselves or their bed partners.

REM sleep behavior disorder is often associated with a neurological disorder, such as Parkinson’s disease or a brain stem tumor.

The Neural Bases of Consciousness

The word consciousness refers to a state: a person is conscious or unconscious.  The term is also used to indicate a sense of conscious experience, or awareness of something.

Consciousness involves short-term memory, and fully conscious humans have a sense of self, which requires long-term memory.

Consciousness varies in level, with coma and deep anesthesia on one extreme, alert wakefulness on the other, and sleep in between.

There are also altered states of consciousness, including hypnosis, trances, and meditative states.

We will consider three components of consciousness here, awareness, attention, and sense of self.

As an abstract concept, awareness is difficult to define and more difficult to study.

Awareness is difficult to define and study, so researchers have focused on awareness of something.

The researchers suggested that the prefrontal cortex might be the key player in producing awareness.

Others have suggested the hippocampus because of its involvement in declarative learning, which by definition involves awareness.

Others claim that the parietal lobes’ ability to locate objects in space is necessary for combining the features of an object into a conscious whole.

The issue of how the brain combines information from different areas into a unitary whole is known as the binding problem.

Numerous studies support the idea that synchronization of activity across brain areas binds the various elements of perception into a coherent cognitive experience. 

Attention is the brain’s means of allocating its limited resources by focusing on some neural inputs to the exclusion of others.

Attention is not just a concept, but a physiological process, and changes in attention are accompanied by changes in neural activity.

When an observer attends to an object, firing synchronizes between the brain areas involved, such as prefrontal with parietal neurons or parietal neurons with visual areas, depending on the task.

When attention shifts, for example during binocular rivalry, activity shifts form one group of neurons in the visual cortex to another, even though the stimulus inputs do not change.

An important aspect of consciousness is what we call the self.

The sense of self includes identity – what we refer to as “I” – and the sense of agency, the attribution of an action or effect to ourselves.

Investigators have found that damage to the anterior cingulate cortex can diminish self awareness, and damage to the right frontal-temporal cortex may produce a detachment from the self.

Farrer and Frith and their colleagues suggest that the sense of agency is mediated by the anterior insula and the inferior parietal area. 

Body image contributes to a sense of self because we have an identification with out body and with its parts.

Without long-term memory it is doubtful there can be a self, because there is no past and no sense of who the person is.

Patients like HM, deprived of short-term memory but with most memories of their past intact, may have a strong sense of self.

Korsakoff’s and Alzheimer’s patients have more extensive loss of past memories, and may suffer greater impairment of their sense of self.

A sense of self requires the distinction between our self and other selves and, arguably, some understanding of other selves.

Some researchers believe mirror neurons are critical to developing the ability to attribute mental states to others (theory of mind).

In Chapter 3 a description of a surgical procedure that separates the two cerebral hemispheres by cutting the corpus callosum is discussed.

This surgery is used to prevent severe epileptic seizures from crossing the midline and engulfing the other side of the brain.

Split-brain patients also raise important questions about consciousness and the self.

There are two competing interpretations of the results of split-brain research:

The language-dominant hemisphere is conscious, while the other hemisphere is a non-conscious automaton.

Each hemisphere is capable of consciousness, and severing the corpus callosum divides consciousness into two “selves”.

Gazzaniga says that the left hemisphere contains a module that he

calls the “brain interpreter.”

The role of the brain interpreter is to integrate all the cognitive processes going on simultaneously in other modules of the brain.

Another disorder of self is dissociative identity disorder (formerly known as multiple personality) which involves shifts in consciousness and behavior that appear to be distinct personalities or selves.

The causes of this disorder are not understood, but 90 to 95% of patients report childhood physical and/or sexual abuse.

Most therapists believe that the individual creates alternate personalities (“alters”) as a defense against persistent emotional stress.

The alters provide escape and, often, the opportunity to engage in prohibited forms of behavior.

Most neurobiological theories of consciousness assume that consciousness requires a widely distributed neuronal network.

According to some theorists, consciousness occurs when the functioning of widespread networks becomes coordinated, enabling them to share and integrate information.

Distribution of consciousness means that there is no center of consciousness, but some researchers believe there must be an executive, an area that coordinates or orchestrates the activity of all the other structures.