This is an archive version of 'Psychedelic Information Theory' Alpha chapters. The final version of this text can be found at:

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Chapter 10: Psychedelic Information Theory

Now that we've seen a little about how the brain is networked, let?s take a moment to look at the root of what we perceive as reality, and that is the combined signal from our sensory inputs. Our senses are the first and last interaction our brains have with actual hard objective reality, and the unique picture we all produce in our minds comes directly from the environmental data gathered by our senses. Though it may seem like unnecessary material to cover, I would like to take a moment to look at each sense a little closer to see what is really going on as reality filters its way towards the abstracted versions of reality we construct in our mind's eye.

Touch

Perhaps the oldest and most basic sense, our sense of touch gives us a direct assay on environmental temperature and pressure, and by direct analysis of those two things infer texture, erotic sensuality, and other raw somatic sensation such as tingling, flashes, itching, pain, etc. But temperature and pressure is what the sense of touch is all about. Our physical detection of radiant energy (heat) is good for finding sunlight (or other sources of warmth) even when blind, and the ability to sense pressure (mass, weight) helps us know which way is up, helps us find our way around obstacles, and provides direct tactile feedback for all motor input and output. And with very fine attunement to our sensory input, our fingers and skin can provide a very crude but accurate molecular assay of particular substances just by touching them and feeling their texture, temperature, and density.

With the exception of sensations that originate around the head and neck, all sensation coming from the body is carried up the spinal cord to the thalamus, which is the central switching station for all incoming sense data (with the exception of smell, which we will get to in a minute). From the thalamus, somatic sensory signals continue upward to an area of the parietal lobe called the postcentral gyrus. The postcentral gyrus is also known as the somatic sensory (or somatosensory) cortex, and is the main cortical processing station for all sensations of touch. This area is slightly back from the top of the head, and corresponds roughly to the "crown chakra" of yogic practice, but instead of being centered on the top of the head it extends down either side of the cortex in a discrete slice towards each ear.

The sense of touch is directly linked to so many basic functions it is hard to imagine existing without it, yet we rarely imagine somatic sensory blindness without a corresponding loss of motor control such as in paraplegia caused by direct spinal cord injury. However, if the science of anesthesia has shown us anything it is that the sense of touch can be turned on and off with a chemical switch, sometimes with corollary loss of motor control, sometimes not. This latter state — a loss of somatic sensory feedback without loss of motor control — is one of the commonly wished-for side effects of low-to-mid range doses of chemical dissociatives such as PCP, DXM, Ketamine, alcohol, GHB, nitrous oxide, cocaine, ether, and many other painkillers, anesthetics, and prescription pharmaceuticals. All of these drugs work by dampening (inhibiting) sensory signal input, specifically somatic input, at various levels of the brain. Some of these sensory inhibitors are more targeted than others, producing a "high" as the tactile response relaxes and the brain is overcome with a sensation of tingling and weightlessness. Sound familiar anyone?

The ability to inhibit the sensation of touch is also a classic hallmark of psychotic and psychedelic states, allowing the user to commit "superhuman" feats without feeling any pain. Of course, inhibiting tactile feedback while simultaneously stimulating the body's adrenal response is a classic hallmark of the "fight" end of the primal "flight/fight" autonomic response to danger, and drugs which mimic this behavior (such as PCP) can be very dangerous indeed. At the extreme end of this spectrum the user can become a wild beast capable of feats of animal athleticism — and this is certainly one possible known side effect of psychedelics like LSD. However, psychedelics have also been known to extremely enhance (stimulate) the sense of touch — making textures stand out and enhancing sensuality, even generating tactile hallucinations — which means there must be a dynamic effect occurring here that goes beyond simple gating or amplification of incoming tactile input. In short, psychedelics may have a simple dissociative effect on tactile input, but may also produce signal distortion or amplification further along the tactile sensory processing regions of the higher brain, creating a dynamic and multi-layered range of tactile stimulus being generated in the psychedelic state at any one moment. We will address these concepts in some depth when discussing somatic phenomena in detail later in this section.

Taste

It is best to discuss taste in the context of the sense of touch because taste is a very refined specialization of the sense of touch. The tongue can discern molecular structures of specific materials on contact: sugars and starches taste sweet; minerals taste salty; acids taste sour; fats taste greasy; water and proteins taste neutral; metal tastes metallic. We have a nice lab of enzymes and acids in our mouth to help break all that info down for further analysis, so when we "taste" something on the tongue we are actually perceiving the chemical reaction of the substance in the mouth with mucous and saliva. The shape and texture is important for determining what the object is, of course, but to "taste" an object is to do a crude chemical assay of the molecule right on the cellular membrane.

When something hits our tongues, mucus and saliva dissolve away what they can and filter the particles into the tiny flower-petal-like taste buds. These little taste pores have extremely tiny "gustatory hairs" at the bottom that send nerve impulses to the brain when they are tickled. These impulses race along what are called special visceral afferent neurons to the brain. The taste buds on the front two-thirds of the tongue are associated with the facial nerve, which is the primary neural pathway for mediating taste sensation and glandular response to taste (such as salivation, oral and nasal mucous production), as well as most facial movements. The taste buds on the back third of the tongue are more closely associated with the glossopharyngeal nerve, which also mediates sensation from the throat and roof of the mouth, and mediates motor control over actions like swallowing and gag reflexes (not to be confused with the vagus nerve, which mediates digestion and vomiting). Both of these nerves pass through various ganglia (nerve bundles) and ascend upward to the brainstem, both attaching at the same area of the lower pons/midbrain area called the nucleus solitarius, which then carries the signal to the thalamus for further routing. From the thalamus, taste sensations proceed upward to the primary gustatory area of the postcentral gyrus in the parietal lobe — the same area where other somatic (touch) sensations are processed, though taste has its own specialized little clusters that are slightly lower on the somatic map, located approximately just above either ear.

Since we are creatures of logic and abstraction, the sense of taste is often taken for granted and may seem like an odd thing to discuss, but it is one of the more refined senses we have, and in reality it is the shaman's best tool for performing crude biological assay of plants and chemicals on the spot. Of course the amount of LSD you would need to get a "taste" of it would be way more than enough to get you high, so for refined pharmaceuticals you should be sure to sample no more than a few grains, and even then look out. But in the realm of phenomenological significance the enhancement of the sense of taste under the influence of classic psychedelics like LSD is commonly reported, yet rarely do people say that their sense of taste is gone altogether. Also, it is reported that objects feel "strange" in the mouth, either too big, too small, or sensation from the tongue is distorted so the user is stuck with the uncomfortable fact that they cannot identify what is going on in their mouth. So it can be said that psychedelics at least have an amplifying effect on gustatory response, with some elements of distortion and dampening effects. Also, gustatory synesthesia, or having other sensations like smell, sight, sound, or touch overlap with those of taste (i.e. tasting a wall with your fingers, tasting the color blue, etc.) are a common side effects of LSD as well. We'll discuss these phenomena a bit later when we talk more about somatic sensory amplification and synesthesia.

Smell

Like touch and taste, taste and smell go hand in hand. It is hard to imagine taste without smell, and smell is one of the most powerful senses we have. Like the sense of taste, the sense of smell is created by a crude molecular assay of gases and aromatic compounds that hang suspended our gaseous environment. It is a very ancient sense, and specific smells can evoke very primal responses (hunger, fear, lust) or evoke profound memories. And unlike all other senses, the sense of smell is not routed through the thalamus, but instead enters directly into the front of the brain through the olfactory nerve, where it diverges to many different areas of the limbic system and cortex for further processing.

The sensation of smell begins when molecules suspended in the air are inhaled into the nose and trapped in a mucous layer at the roof of the sinus cavity. When a significant amount of any substance is trapped, two tiny receptor patches (or epithelia) begin sending signals to the olfactory bulb, which acts as a data pre-screening hub. The olfactory bulb then sends the signals on to the olfactory nucleus, which in turn sends signals through three different nerves into various areas of the brain. The medial olfactory stria sends signals to areas of the limbic system, including the septal nucleus, hippocampus, the hypothalamus and upper brainstem, and is no doubt responsible for many of the primal hunger and memory responses to smell. The lateral olfactory stria diverges into the primary olfactory cortex, which is located in the very forward, inward part of the temporal lobe, and is no doubt where the bulk of our "sensation" of smell happens. It is also no surprise that the lateral olfactory stria also diverges into the amygdala, making its emotional integration with the limbic system very tight. And if there were any doubt as to the primacy of smell over our emotional response, the final olfactory stria sends signals to the olfactory tubercle, which is located in an area of the basal forebrain called the anterior perforated substance. The olfactory tubercle also receives input from the dopaminergic neurons of the substantia nigra, as well as neuronal input from the visual processing system, and is implicated in the rewarding effects of cocaine (along with the nucleus accumbens, which is also implicated with reward, pleasure, and addiction). The actual function of the olfactory tubercle is still not known, but judging from its placement and the connections with dopaminergic modulators and visual signals, it is safe to say that it plays a strong role in integrating the sense of smell into mood and behavioral response, presumably in the context of pheromone response, mating, and sexual reward.

In relation to psychedelic experience the effect on the sense of smell is either very small or regrettably under-reported. The reporting of olfactory hallucinations is not unheard of, but it is rare or typically a small side note in otherwise detailed reporting. I would find it hard to state one way or the other whether psychedelics had any influence on the sense of smell at all, other than the odd report of olfactory synesthesia, such as a smell producing a visual response, but very rarely is the reverse true, such as a sound or color producing an phantom smell or olfactory effect. Personally I have found the sense of smell under psychedelic influence to be generally unaffected, but my body's response to smell stimulus is more acute. For instance, a rose may smell no stronger under the influence of psychedelics than before, but the joy or memory response produced by the smell may be amplified ten-fold, meaning that there is probably no gating or amplification of olfactory input per se, but there is likely an excitation of olfactory sensory processing going on at some level up the sensory processing pipe. We will examine this idea in more detail when discussing synesthesia and emotional response in later sections.

Sound

Sound is a complex sensation derived from the processing of standing wave formations in the air within the range of around 20 to 20,000 Hz (hertz, or cycles per second). Using a refined mixture of detection techniques for sensing changes in atmospheric pressure as well as gauging angle, direction, and strength of incoming signals, our sense of sound is generated via three things simultaneously: vibrations in the air and ground felt by our entire bodies; targeted vibrations that echo off the shape of our cranium; and even more targeted sounds that bounce along the curvatures of our ears into our inner ears and focus like a lens against our eardrums. Our eardrums — those simple-looking membranes of stretched skin — hide what may easily be the most sensitive register of atmospheric disturbance ever devised: the inner ear. The inner ear is capable of discerning minute shifts in pressure, volume, and activity in the atmosphere; is crucial in mediating balance and spatial orientation; and is capable of simultaneously "listening" to many distinct sounds, patterns, and standing wave formations all at once (while conversely filtering out pre-selected irrelevant noise and data). The ears do more than just hear: they fine-tune our abstraction of reality, focus our attention, and keep us immersed in the now (even when our eyes are closed).

If you think the sensations of taste and smell are complex, they've got nothing on our sense of sound. While the processing of sound in the cortex is essentially the same as any other sense, the mechanisms in the inner ear which translate sound into neural impulses make up one of the freakiest, Byzantine, and most surreal Rube Goldberg machines I have ever seen. Up to the eardrum everything about the ear seems normal, but once you pass through the tympanic membrane you're essentially 500 million years back in the Cambrian era. The inner ear is a salt-water filled cavity. Since sound vibration does not carry through fluid very well, a little hammer (malleus) attached to the tympanic membrane strikes an anvil (incus) with a Morse-code-like compression of tympanic vibrations that are then passed to a stirrup (stapes) which vibrates against the oval window on the outer membrane of the vestibule, which acts as an internal amplifier and translates oscillations from the oval window into fluid pressure within the bony and membranous labyrinths of the cochlea (whew!). The cochlea itself — literally "snail" in Greek — looks like a snail shell wrapped around a bony spike, and the circular chambers within the cochlea respond to fluid pressure generated in the vestibule. Fluid pressure variance in the cochlear canals transmits signals to the organ of Corti, the cellular membranous structure which houses the sixteen-to-twenty thousand fine hairs of the inner ear. In short, our sense of sound is generated by ripples in fluid pressure tickling the tiny hairs up and down the nautilus-like interior canals of the cochlea.

If you think back to the "brain as ancient sea creature" metaphor in the section on neurons, it is easy to see how the particulars of the inner ear are constructed out of very basic and ancient evolutionary things — salt water, tubes, channels, membranes, hairs — and the awareness of ripples and pressure variance provided by these things are all essential to survival on the deep sea floor. The very nautilus structure evolved in the seabeds, and probably appeared in microscopic form long before that. The spiral form was no doubt both cheap to develop (in evolutionary — or energetic — terms) as well as instrumental in detecting the various narrow-range vibrations of potential food sources along with the various long-range vibrations from large hungry predators wriggling up for a better look.

From the cochlea, signal from the inner ear moves along the auditory nerve and joins with the brainstem at the upper medulla and lower pons. From there it interacts with the olivary nuclei and moves up the brainstem in a cascade of serial and parallel processing networks that integrate pitch and intensity data, diverge, adjust for stereo distortion and time delay, and then re-converge in the inferior colliculus on the pons to "localize" the sound in 3-D space before passing the signal upwards to the medial geniculate bodies on the underside of the thalamus for further routing up to the primary auditory cortex in the temporal lobe. There is a patch on the left audio cortex of the temporal lobe called Wernicke's area, which specializes in processing grammatical syntax and language, and it also works in concert with Broca's area in the frontal lobes for formulating and feeding syntactical language structures to the primary motor cortex for relay to the tongue and lips. In contrast, the right auditory cortex is more attuned to the underlying rhythms, harmonic overtones, and emotional context of incoming sound signals (Left Brain vs. Right Brain lateralism again). Since speech, singing, dancing, and the production of music are all motor activities, many areas of the auditory and language cortex are also cross-wired into the motor cortex, allowing you to simultaneously process language and music while keeping up at the correct pitch tempo; whether you're conversing, dancing, tapping your foot, singing along, etc.

Since so much of language and music and environmental processing depends on our sense of sound it is no wonder that it plays such a large part in the content of the psychedelic trip. Of all the senses that set the tone or context for a psychedelic trip there is none more powerful than sound. The experienced tripper knows that having the right music available and prepared before going into the trip is essential for mediating the smooth transitions between various psychedelic mind states. And at the risk of revealing one of the keys to this whole text, it is my assertion that sound is the primal medium for modulating the entirety of psychedelic action, and is at the heart of all successful shamanic methodology. Through sound, music, and language, the brain can be stimulated in almost every way: and in the psychedelic realm, the sense of hearing/sound is enhanced to the extreme. Many things can be going on in the audio realm: the loss of white-noise screening; audio babble; voices and audio hallucinations; audio synesthesia; audio distortion; echoes and loops; acute sense of hearing; transliteration (the mixing or misinterpreting of incoming language signals); etc. And since so much of the mind's dialog is internal, when the audio signal processing becomes distorted it is difficult to tell where the external audio sources end and the internal audio sources begin. This is why one of the shaman's greatest tools is music — be it bone-rattle, drum, atonal drone, jam-band, or turntable. Music and rhythm keep the mind grounded in the moment, set the tone for the trip, and can carry psychedelic vibration from one state to the next very rapidly. Of course, we will be discussing sound and psychedelics in much detail throughout the course of this text.

Sight

Sight is the most discriminating of all the senses, taking input in an extremely tiny range of photonic radiation from roughly .7 to .4 micrometers in wavelength (also known as infra-red to ultraviolet radiation, or the visible light spectrum). And it really is a tiny sliver of the entire spectrum of energy all around us, a discrete rainbow palette for rendering the shape and color of all things that absorb and reflect the sunlight (or simulated sunlight). The visual signal starts as concentric rings of photonic data absorbed by the retina which then move in impulses along the optic nerve. The retinal image is captured upside-down, but when the image hits the visual cortex in the occipital lobe (the back of the brain), it is flipped vertically and the raw data gets translated from concentric rings into the neat angular lines, fills, patterns and shadings that make up our typical 3-D representation of reality. Within the process there is line discrimination, shade discrimination, color discrimination, depth perception, movement perception, blind-spot and periphery filling, not to mention all the emotional, logical, and symbolic parsing that needs to happen when encountering letters, words, charts, faces, works of art, language, numbers, symbols, etc.

In contrast to the routing of audio signal, the brain's visual system is quite neat and tidy. Binocular vision tapped in the retina is stereo-matched when the optic tracts from both eyes cross and intersect in the optic chiasm, where monocular data enters from either side but splits and diverges with binocular data. This binocular data is the sent to both the brainstem and the lateral geniculate nucleus (LGN) on the undersides of the thalamus for further routing to the visual cortex in the occipital lobe, where the bulk of our visual processing and filling is done. Primary visual data undergoes some basic signal screening and processing in the LGN before being passed back to the visual cortex, and signals that move from the LGN to the visual cortex are routed along two paths: while the first carries the bulk of sight data directly back to the visual cortex, the other pathway (which carries data only from the upper and outer regions of sight) takes a detour through the temporal lobe along what is called Meyer's loop.

Many visual signals don't ever make it to the visual cortex, and diverge away from the cortex to the brainstem (particularly to the superior colliculus) to help mediate the pre-cognitive sensory feedback between sight, involuntary eye movement, visual focusing, involuntary startle responses, and the tracking of moving objects. Involuntary pupillary dilation and light response are also mediated via pre-cognitive brainstem feedback through the pretectal nucleus, which is also under the thalamus on the front side of the brainstem.

In addition to the primary focal pathway and the involuntary feedback pathways, there is also an ambient pathway to the visual system, which is primarily responsible for processing movement in the periphery of vision and maintaining our sense of movement and orientation in space. In the ambient pathway, neurons carrying information from the periphery of the retina diverge into the brainstem and join with the sensory motor pathway in the parietal lobe to effectively coordinate our movements in reaction to what is going on in the space around us.

Between the brainstem, the LGN, the visual cortex, and beyond, there is a lot of articulated scanning and analysis of visual data going on, but these processes are all very specialized and localized; and the pathways are very simple. Since hallucinogens have such a profound affect on visual and spatial perception, it is assumed that areas that process visual and spatial data (thalamus, brainstem, and cortex) must be implicated in hallucinogenic effect. Of course, when you are talking about the thalamus and the brainstem and the cortex you are basically talking about the entire sensory processing system, and since most senses follow the same schematic it can be assumed that any substance that interferes with one of them will likely interfere with all of them. The organs that process sensation are alike in both form and function, and have discreet interplay with each other to create the gestalt of reality in our higher cortex. Any disruption in visual processing functions will of course have a corresponding effect on visual perception; but the same disruption will likely have an effect on sound processing and perception as well. Like smell and sound, sight is wired into so many areas of the brain that a disruption in signal at any one area could have a cascade of perceptual effects all over the brain. If the functioning of the higher cortical circuits that analyze any of these essential sensory data were disrupted or stimulated in any way, the range of corresponding perceptual effects would be extreme.

To most of us sight is reality, and "seeing is believing." We don't ever stop to think that our most reliable sense could fool us, and when it does our first response is (of course) disbelief. And when you alter your sense of sight you fundamentally alter your sense of reality. You can have audio hallucinations and easily dismiss them as just in your head; if you can't see the source of the hallucination, it doesn't exist. However, if you see something in a hallucination, it is very hard to discern whether it does or does not exist, because the typical visual logic gets overruled. Even if it was a hallucination, your brain rendered it as real in your mind; and your memory of it is also real, so trying to figure out what is real and what is not comes down to a semantic exercise that only runs you in circles. But my point is this: visual confirmation of an event is often thought of as the same thing as "reality" to most of us, so bending visual reality is often misinterpreted as bending actual reality in the mind of the psychedelic user, because if you see it with your eyes it's real, right? Well no, not always. Actually almost never. What you feel when you are hallucinating is real, and what you remember is a real memory of an actual perceptual event, even if what you saw in that event was most likely a complex illusion.

As we have already discussed briefly, the brain also has its own internal sight that renders dreams and the imagination for the mind's eye. This should not be confused with the visual sensory system, though both feed into the same emotional and analytical areas of the brain for further processing. It is important for the purposes of this text to distinguish between these two distinct senses of "sight," for it is my estimation that different hallucinogens produce vastly different visual effects based on which one or combination of these different senses they distort or stimulate. Dissociative dream hallucinations are different from tryptamine-induced perceptual distortions, though there is an area in the middle where the two can overlap quite seamlessly. But in order to make a clear distinction I have classified the two types of hallucinatory states as "Open Eye" and "Closed Eye" visual phenomena, even though either can occur when eyes are open or closed depending on the dose and substance you take. The main difference I want to make between these two types of visual hallucinations is that Open Eye visuals refer to signal distortions happening within the visual light processing system (such as light trails, spatial distortions, crawling textures, etc.), while Closed Eye visuals refer to those which are generated internally by the mind's eye (such as phosphenes, phantom faces, or fantastic imagery). We will of course be discussing both of these visual systems (as well as the other senses) in more detail in the next sections.

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