The HumanNervous System

Every morning, or around about then, a miracle happens. You wake up. You were asleep, dreaming perhaps, oblivious to most sensory input. Then the dial gets turned up, either quickly or gradually, and you become more aware of your environs. You get up or you lie there thinking about your day. What is happening in your brain? Let’s look at the neurobiology of sleep, dreams, and unconsciousness, to see if we can learn something about the nature of the self, the phenomenological experience I’ve been calling consciousness. The ghost in the machine.

Brain activity is different when asleep than when awake. Consciousness is also different, not merely absent. Counter to intuition, there is more brain activity when at rest than when concentrating on a task, at least more of certain kind of brain activity. The brain is not turned off in sleep, the volume knob is not turned all the way down. Some marine animals and birds turn down one side of their brains at a time during sleep, keeping one eye open as they say.

Brain activity while dreaming resembles waking activity. Dreams mostly occur during REM sleep, so named for the rapid eye movements that can be seen in a dreaming person. Dreams can also happen in NREM sleep, and in-between stages of sleep. In fact, thinking of sleeping in stages may not be the best way to characterize the brain activity. The dream world experience and the real-world experience are created by the same machinery, differing only in the network activity.

We often remember and think about our dreams. Our dreaming conscious awareness, our dreaming phenomenology, shares several features with our waking phenomenology. The conscious experience of the dream has visual and auditory components. There are objects and events from daily life, animals, people, buildings, social situations. Sometimes it’s hard to tell if you’re dreaming or awake. We have work dreams. Stress dreams. Sex dreams.

The dream world can also go beyond the mundane of everyday life and existence, beyond the boundaries of physics and earth. Images and thoughts from the day can be randomly combined with memories, fantasies, and fears. Dreams can be a vivid hallucinatory experience and remembered as directly experienced, not like thinking about a memory. What are they for? Do they have a function? These phenomenological resemblances and differences come about from the overlap of awake and asleep neurological states. There is another state we should consider that is neither sleep or awake – general anesthesia.

The anesthesiologist does not put you to sleep. She does not put you under. With the right cocktail of drugs, she completely alters your perception, memory, and consciousness. These two states, anesthetic and asleep, also share neurological mechanisms. The two states differ in perception of pain (analgesia), ability to move (akinesia), and anxiolysis. Anxiolysis is an unconscious state where the person can hear and understand and follow simple directions with usually no memory of the procedure. General anesthesia is not sleep, it is not wakefulness, it is not dreaming, but introduces another neurological state to help us triangulate on consciousness and the self.

We are very good at pharmacologically manipulating consciousness, and we have been very good at it for a long time. Some people are better than others. In hospitals, labs, taverns, and at home, we alter consciousness with elixirs, potions, and drugs. We alter our minds with a chemistry set.

Let’s look at the neuroanatomy. The hypothalamus, as you recall from previous posts is a triangular sheet of neurons hanging off the thalamus. The hypothalamus is a visceral processing hub, and the thalamus is a somatic processing hub. Certain nuclei of the hypothalamus play an important role in controlling sleep. These nuclei contain pools of nerve cells that respond to light cycles affecting sleep and arousal. The superchiasmatic nucleus of the hypothalamus, named for its location just above the optic chiasm, uses light information to set our circadian rhythms, an internal clock. We’ve already talked about the preoptic area of the hypothalamus that sets puberty and our sexual clock. The hypothalamus also controls the pituitary gland.

The thalamus relays information from the senses to the cerebral cortex. The thalamus is the dial, turning up and down sensory input, disturbing voluntary control of the muscles. With somatosensory input and motor output squelched, the sleeping brain can turn to internally generated images and sounds. The pineal gland, located deep within the brain, releases melatonin, a hormone that increases with darkness and promotes sleep. Now we can sleep and dream.

Brain monitoring and imaging studies show that brain activity, and the location of that activity is very similar for awake and dreaming participants. For example, occipital lobe activity and activation of the ventral visual stream are seen when participants are in REM (rapid eye movement), when most dreams happen. Additionally, there is increased limbic system activity during REM. As you recall from previous posts, the limbic system is a neural network of connected structures linking the hippocampus (memory) with the cingulate cortex (emotion). Other structures in that neural loop (the Circuit of Papez) are the mammary bodies (short term memory), the thalamus, to gate the circuit, and the amygdala. We already discussed the role of the amygdala in sex and violence, and dreams can have violent and sexual themes and images. Additionally, the hippocampus’ role in this dream neural network, and in waking imagination, is to provide memory context to construct novel situations and potential or even desired outcomes. Is this evidence for a function for dreams, a reason for dreams?

A quick caution in our line of thinking. If we decide that dreams have a function, it does not mean that dreams evolved for that function, nor does it mean the function is beneficial. Dreams can be random combinations of pieces of visual and emotional memory, as our brains clean house and organize files. Dreams can be that, and they can have functions, be sometimes meaningful in our daily lives. Or a function could be self-entertainment while we sleep.

Norepinephrine and serotonin levels are reduced during REM, which calms and slows the body. For most of the time in REM, our bodies are lifelessly paralyzed, unable to move. Perhaps you have felt this in a dream, when you could not run, or could act. During REM, the dopamine circuit lights up, perhaps suggesting a reward function for dreams, or a reinforcement of some other neural process. Dreams can also be frightening and horribly sad. Why would our brain reward and punish us in our sleep? Why not just work those things out when you are awake? If dreams are sending us a message, who is the sender and who is the recipient? It would seem one pattern of activation, one active network to another. Dreams can be rewarding, heavy, meaningful, or random without having to invoke a self that is fractured into id, ego, and superego.

Studies with brain lesion patients and with epileptic patients show that the neural machinery for dreams is more related to imagination than perception. Imagination is a top-down process, progressing from higher order cortical activity to specific sensory experiences while perception is a bottom-up process starting with the sensory experience and progressing to cortical activity. This suggests that a higher order network, unrelated to attention, is the source of the dream. Our dreams are, in a very real sense, an extension of ourselves.

I have proposed in The HumanNervous System – The Human Nervous System in Everyday Behavior (thenervoussystem.blog) that emergent properties, synchronized brain activity across large areas, are the origin and constitution of consciousness and the self (in the phenomenological sense, not just awake and aware consciousness). Dreaming also seems to involve emergent functional states. Emergent networks activate an internal world, while suppressing the external one. You experience this. You are in it, not just looking down on it. Then the hallucination is over, the networks are off. The waking brain and the sleeping brain exhibit different patterns of neural activity. These emergent networks specifically connect the processing power of the different neural structures and pathways we have been talking about. The sleeping network harnesses the hippocampus, the amygdala, the language centers, and the occipital lobe to perform functions exactly as they do when you are awake.

Being awake and being asleep are states that overlap, for example when you are trying to wake up, when you are daydreaming, and when your mind is randomly wandering. We would expect the network to overlap as well, and they do.

Let’s go back to our drug cocktails used in general anesthesia, the state that is neither awake nor asleep. Drugs such as propofol disrupt nervous system activity synchronization, shutting down the emergent states. They sedate the patient, inducing unconsciousness and inhibiting dreaming. During this dissociate state, the cortex and deep brain structures do not communicate. In neuroscience terms, there is cortical-subcortical decoupling during induced unconsciousness. Like an on and off switch, the synchronized activity, the higher order processing you might say, turns itself off only later to turn it back on again, switching states.

This dissociation is different from the thalamic and hypothalamic control of sleep, where the transition to sleep is a graded reduction of processing the external environment. The volume knob is not turned down, the network is turned off. Where does the ghost go when this happens? What happens to the self? Are we zombies under anesthesia?

Brain imaging studies, for example, functional MRI (fMRI) studies have shown that not all synchronized activity is decoupled. When the brain is at rest, or lost in random thought, the pattern of activity is called the default mode network. This network is hypothesized to be linked to mind wandering, daydreaming, and internal imagery. Anatomically, this network involves the posterior cingulate gyrus, the medial prefrontal cortex, and the angular gyrus. This network seems to be active when thinking about the self and thinking about others. In other words, a social cognition network.

Psychologists call this type of thinking Theory of Mind. Theory of Mind is the developmental capacity to understand that others have a mind, and can hold different perspectives, beliefs, intentions, and emotions. We’re going to need another blog post to talk about Theory of Mind. Disruptions of this network have been hypothesized to be involved in the autism spectrum, as well as other conditions that involve a disruption of social processing, for example schizophrenia and major depression. We can look at these conditions as within the range of natural neural processing, and not as neural deficits.

The default mode network, with its connections to language comprehension centers, vision centers, and internally focused processing could be the source our internal dialog (Menon, Neuron 2023). This internal voice is a running narrative, an experience of subjective continuity. Menon goes on to postulate that this narrative is fundamental to the construction of our sense of self, that it shapes our social cognition, and forms a vital component of consciousness. Have we found the neurological basis for the self? For the ghost?

In the next blog post I will look at some of the disruptions of consciousness and social interaction including traumatic brain injury, the autism spectrum, and attention deficit disorders. These perspectives will focus our search and refine out thinking about the self and conscious phenomenology.