Sleep Paralysis Causes Next Day Distress

What about the Next Day? 

What if I told you that this fun little experience of Sleep Paralysis actually did affect you. What if your emotions, personality, and general demeanor were completely altered. While reading Science Daily last week, I stumbled upon a very interesting article on Sleep Paralysis. Two researchers, James Cheyne and Gordon Pennycook, released findings from a study in the Clinical Psychological Science Journal, concluding that Sleep Paralysis affects an individuals’ interactions with the world the next day in a negative way.

The Study

By using an online survey and follow-up emails, the two researchers collected information from 293 people  to explore post-episode distress by measuring a range of items. They measured different characteristics relating to the episode itself, such as amount of fear experienced, vividness of experiences, frequency of episodes. They also looked at factors relating to each individual, such as psychological distress sensitivity, supernatural beliefs about the Sleep Paralysis experience, and cognitive style (either fast/intuitive thinking or  slow/reflective/analytic thinking (Evans, 2008)).

The Findings

Concurring with their proposed hypothesis, the researchers found that the characteristics of the episode directly related to the amount of distress the next day. The more fear experienced during the episode, the more distress an individual felt the next day. The distress was further exacerbated in those who felt fear of threats or assault, such as chest pressure, intruders, and near-death experiences. The distress was also worse for people who felt sensations of floating, falling, or out-of-body experiences (Cheyne, 2013)

The researchers also found that an individuals level of psychological distress (anxiety, depression) had had almost no effect on the amount of fear experienced in the episode, although it still resulted in post-episode distress.

Individuals who held supernatural beliefs about the Sleep Paralysis experience reported increased intensity of both fear and threat/assault experiences as well as increased postepisode distress compared to others. Additionally, those with analytic cognitive styles were found to have significantly less supernatural beliefs about the experience. This makes sense, for people with analytical thinking styles would reach out to others for more information and explanations on the experience, dissuading them from supernatural interpretations (Cheyne, 2013).

Surprising to the researchers and myself, those who employ more analytic cognitive styles of thinking experienced noticeably less distress after the Sleep Paralysis episode. Although the above findings directly show this, these results now show the ability of executive control processes in our brains to inhibit, activate, or manage more automatic processes, such as emotional reactivity after the episode. Therefore, analytic people are more likely to override their postepisode feelings of distress.This is further  supported by the findings that individuals the cognitive style had no affect on the  level of fear experienced during a particular episode (Cheyne, 2013).

What Are The Implications?

There are many important implications of this study. According to a post in the Toronto Telegraph, the researchers believe that “the distressing sensory experiences that come with episodes of Sleep Paralysis could exacerbate people’s fear, creating a feedback loop that enhances memories of experiences later”. This is very well supported from the results presented above, for analytic people must inhibit part of the loop preventing the enhancement of the memory later on.

Although a little far-fetched for the current amount of knowledge on Sleep Paralysis, the researchers also emphasize that studying these carryover effects further could “make a significant contribution to the billions of dollars, worldwide, in costs associated with accidents, illnesses, and lost productivity associated with sleep disturbances.”

I believe them- they’ve definitely found interesting correlations, and I applaud them for what they have found- but A LOT more research from other fields-like Neuro- will definitely be needed to truly achieve this goal.


Chest Demons Revealed- The Story Behind Sleep Paralysis

The Scary and The Truth

The Experience

As you lie in your bed and feel your muscles start to slowly relax, you expect your mind-wandering off into dream land-to shortly follow. All of a sudden you realize that you are still awake, but you cannot move. Everything starts to spin and distort, you start getting hot, your chest starts feeling heavy, and you start freaking out. Human nature quickly begins to scream at you to escape; to somehow wake up and just end the nightmare. So you-in your completely conscious state-try with all your might to move just one finger, kick one leg, or just swing one arm over your body, knowing your success would bring you back from the mysterious hell in which you’ve found yourself. Welcome to the world of Sleep Paralysis.

The History

First like to start off by stating, Sleep Paralysis is NOT dangerous. Yes, that horrifying, mind-altering experience explained above is not dangerous, nor is it the result of little Incubus demons sitting on your chest as you sleep-Yes, our ancestors really did believe this. Sleep Paralysis is actually a protective mechanism used by our bodies to pretty much stop us from doing stupid stuff to ourselves while resting. You might wonder, Well, how does someone sleepwalk, then? The answer, my friends, is they have a problem with the exact same system that causes Sleep Paralysis: Where Sleep Paralysis sufferers cannot move their muscles when their minds are still awake, Sleepwalkers cannot stop moving their muscles when their minds are asleep.

Behind Paralysis

Sleep paralysis occurs when Peripheral Atonia comes into the dreamer’s consciousness accidentally. Peripheral Atonia is basically a lack of normal tension or muscle tone, resulting in the perception of paralysis. This mechanism is the primary means of inhibiting movements during REM and non REM sleep. Originally believed to be the result of the neurotransmitter Glycine, more recent work has shown blocking Glycine receptors fails to affect Atonia, leaving the mysterious mechanism of paralysis unknown (Brooks, 2008). Furthermore, many people report the eyes to be the only muscles unaffected during the paralyzed state, leaving one able to view the 180 degrees of the visual spectrum, but unable interact with the world around them.

The Phenomena 

Not everyone experiences sleep paralysis,  it could happen only once or many times in a persons life, and can occur more than once during rest. 60% of the population has experienced Sleep Paralysis at least once, whereas 6% experience it quite frequently. Additionally, there are two types: Hypnagogic Paralysis occurs when one tries to go to sleep, whereas Hypnopompic Paralysis occurs upon waking up. Overall though, the most interesting aspect of the experience  is what you perceive, and apparently it varies quite drastically.

Some people hear voices, sometimes of a threatening or terrifying nature, reminiscent of the auditory hallucinations of schizophrenics. Some of the more common phenomena are heaviness on the chest and feelings of suffocation. Other experiences are weird alterations of 3D depth perception, strange or familiar smells or tastes, feelings of levitation, tactile hallucinations, feelings of heat, or visual hallucinations of shadows, people, or intruders (Peters, 2012).

Personally, I have experienced a variety of phenomena during Sleep Paralysis. I’ve heard a woman shrieking, felt my entire body

begin vibrating, seen a shadow of a woman moving towards me in the dark, and quite enjoyed  John Lennon-a black-and-white poster  on the opposite wall of my bedroom- kneeling at the side of my bed upon waking one morning.

The position of  your body, and the timing of sleep can also affect the chances of experiencing Sleep Paralysis (Cheyne, 2002). Many find paralysis most common when they fall asleep sitting upright, an experience that kept my childhood Car and Airplane rides personally quite frightening, while rather entertaining for everyone else. When failing to stop myself from sleeping, I quite successfully astounded others who believed me to be asleep, by regurgitating entire conversations after forcing myself out of the paralyzed state.

The Emotional Effect

Although I’ve emphasized Sleep Paralysis is not physically dangerous, there are emotional implications. The frightening, terrifying, life-threatening, feelings experienced during the Paralysis not only affect an individual at that moment in time, but also affect a persons mentality and emotions afterwards. In the post to follow, I will explore a recent study on Sleep Paralysis, finding that the distress experienced during the event might actually carry over to the next day, affecting your personal interactions with the world around you.

Color Vision: Physics of the Retina Part 2

The Issue of Clarity versus Color

Although surprising, the primary reason for these differing types of photoreceptors is not to perceive colors, but is to accurately see objects, more specifically spatial acuity. Think of a caveman trying to find an apple surrounded by rocks. Although the differing colors would be considered the telltale sign of which is which, detecting the shape and seeing the object clearly, whether close or far away requires spatial acuity. The physics of the retina (the location and spacing of of different photoreceptors) allows us to see objects clearly, and our ability to see colors came as an result of adhering to these necessary physics.I have condensed and added my own insight to an excellent blog post on Visual Acuity, from the blog WebVision, in order to help me explain this intriguing system.

Why not have more Cones for more color?

Based off of what I explained in Part 1, You might ask: Why not have more Cones types to see more colors? The reason is this magical idea of visual or spatial acuity, and the Physics of our retina.

Snellen letters are used to measure visual acuity in target recognition tasks. Each piece of the letter (stroke width and gap width) subtends 1/5th of the overall height, and the entire letter corresponds to 5 minutes of arc. A person with 20/20 vision should be able to read the letter E at 20 feet (6 meteres), where one of the strokes of the letter subtends one minute of arc at the eye. Visual acuity in Snellen notation is given by the relation: Acuity = D’/D where D’ is the viewing distance, and D is the distance at which each letter subtends 5 minutes of arc. Target resolution, on the other hand, has a threshold defined as the smallest angular size at which subjects can discriminate the spacing between the critical elements of a stimulus patternlike a grating.   Screen Shot 2013-03-11 at 12.12.45 PM

Limitations of the Retina

          Our ability to detect fine details depends on two factors, an optics system that combats aberrations, and the spacing and size of our receptors. The optics of our eyes cause distortions, where an object is imaged on the back of the retina as a distribution or point spread function.Screen Shot 2013-03-11 at 2.40.10 PM

           The optics of the eye combats two necessary aberrations that would inhibit spatial acuity.  First, shorter wavelengths of light refract more than longer ones, meaning that Blue wavelengths would be brought into focus infront of red or green ones in the Retina. The eye corrects for this chromatic aberration by placing Blue cones further out in the periphery of the retina, so they refract to the same nodal point as the Red and Green light wavelengths. As a result, Blue cones have larger receptive fields than Red and Green Cones, creating a sort of blue blur. Second to combat is spherical aberration, which occurs from wavelengths of light at the periphery of the lens refracting more than those going through the center. The eye compensates for this by allowing the pupil muscles to contract and dilate, subsequently increasing and decreasing the size of the lens, in order to block unnecessary peripheral rays that would blur the images of varied distances.

Receptor Spacing and Diffraction

          Raleigh’s criterion is used to calculate the resolution of the eye for stimuli that are degraded by these optics. Two points or lines are resolved (are clear) if the peak of the point spread function lies on the first trough of the other point spread function, or when as=1.22L/d, where L is the wavelength of light, and d is the size of the pupil. This means, that two objects must be separated by the width of their point spread functions in order to be seen as two separate objects, if the width is any less, they are seen as a uniform object.

          The spacing and number of Cone receptors therefore affects the quality of the image perceived. Helmholtz proposed that a grating would be resolved if there is a row of unstimulated cone in between rows of stimulated cones (Peters, 2003). In laymans terms, this means that if each individual receptor were to pick up an individual pixel of visual info, the  spacing between adjacent receptors must be small enough and the number of cones large enough (at least in the foveal area) to not accidentally skip over a pixel, which would cause a blur or distortion of the image (ex. seeing the white separate from the black lines in the grating).  Cone spacing at the fovea is approximately 2.5 um (Curcio, 1990), allowing for a maximum of 60 cycles per degree, directly hindering our visual acuity.

Summing it All Up

         Due to the concave shape of the retina, the properties of refraction and diffraction, and the spacing of receptors throughout the eye, there is no possible way to incorporate more colors into our visual palette without hurting our spatial acuity. Creating a different cone type that was tuned to a larger or shorter wavelength, would require an increase in the spacing between adjacent receptors of similar types, a decrease in the size of the receptors, or a decrease in the number of receptors for each respective wavelength. Decreasing the size of the receptors is not logical, and a decrease in the number or increase in the spacing would both directly affect acuity. With regard to optics of the eye, the lens would have to refract even more than it does already or pupil size would be too small or too large to clearly pick up any image.

         For these reasons, we aere left with only Red, Green and Blue Cones. Because wavelengths for Red and Green only vary by 30nms-compared to Blue wavelengths-we are able to have three types of cones, instead of just two. Therefore, in a sense, our ability to evolve towards only trichromatic color vision is a quite ingenious solution to a rather complex problem: color versus clarity.

Color Vision: Perception in the Retina, Part 1

How do we really see colors?

           How do we perceive colors?  Ever questioned how so many people can be colorblind, yet still see perfectly?  Recently, in the article Time to Get Real: The Riddle of Perception, by The Huffington Post, our unique ability to perceive color is touched upon. After reading it, I felt it necessary to spend the time to explain to you just how interesting the phenomenon of color perception actually is, and how “color” perception actually comes second to shapes.

Our ability to see a range of colors (although quite small) is the result of a series of stages of processing, involving both feedback and feedforward mechanisms. Light (an electric signal) from the external world gets converted into a chemical signal by neurons in our Retinas, and are processed through pathways in the brain. These subsequent processing stages, where our neurons “detect” edges and borders by comparing contrast, eventually result in the perception of both objects and colors.

Primitively, discriminating between different objects of varying size, shape, and color was necessary for survival, especially in determining ripeness of food. Scientists have believe there to be an ancient universal color system among Vertebrates, in which all had 1 pigment gene with a absorption <500nm, one with an absorption >500nm, and Rhodopsin (Nathans, 1999).This primitive system has evolved through either gene duplication or a polymorphism, and resulted in the different species with different numbers of pigment genes, leading to the detection of a spectrum of colors. Therefore color vision, while originally meant for determining basic contrast differences for survival, has evolved to enhance our perception of objects in world. The ability of Humans to see visible light completely depends on only four different types of pigment genes that respond best to four wavelengths of light: Red (559nm), Green(531nm), and Blue(419nm), and Rhodopsin (496nm) (Nathans, 1999).

I have decided to explain this phenomenon of shape and color perception in two parts. In the first part, I will explain how neurons in the Retina perceive different hues, and how the activation of only a few types of cells results in our perception of a spectrum of colors.  In the second part, I will explain how physics actually comes into play, and directly results in a sad, but necessary trade-off between excellent perception of shapes, and lack of perception of a larger spectrum of colors.

Neurons in the Retina Compare Signals 

The retina consists of four different types of wavelength-sensitive sensory receptors. These sensory receptors are called Photoreceptors. Photoreceptors activate (or hyperpolarize, to be exact) when a photon of it’s preferred wavelength contacts it. This results in a cascade of events, that eventually, upon reaching higher processing levels in the cortex, results in our perception of objects, colors, and space.

The four types of photoreceptors can be split into two groups: Rods and Cones. Neurons called Bipolar Cells compare the inputs from different Rods and Cones in order to distinguish different hues. After that, neurons called Ganglion Cells further compare the bipolar cell inputs, and send information to the brain, as the 1st of many steps towards perceiving the visual world around us.

From Light to Neural Info

Rods are larger and more numerous than cones. Rods use the ancient pigment gene, Rhodopsin, and are not very sensitive to light (it take 10 photons for a response), but once activated, they can take up to an hour to return to normal levels in order to capture more photons. Therefore, having 120 million of them-compared to 3 million Cones-is quite useful.  Rods saturate (reach maximal sensitivity) around 496nm, making them good for detecting objects in dim light levels and darkness (Naarendorp, 2010). Their low saturation level and their abundance in the outer retina makes them more useful for luminance instead of shape perception (spatial acuity)…I will explain more about this in Part 2.

On the other hand, Human Cones respond to longer wavelengths, and never saturate, making them useful to perceive colors, objects, and the visual world. There are three types of Cone pigment genes, or Cones: L Cones (Long wavelength or “red” sensitive), M Cones (Medium wavelength or “green” sensitive), and S Cones (Short wavelength or “blue” sensitive). Cones are abundant in center of the retina (the fovea) to about 10 degrees out from the center of vision. Cones are therefore what we use in normal and bright light conditions and for visual acuity (seeing things clearly) (Li, 2010).

Comparing Different Signals Through Processing Levels

This interesting task of comparing wavelengths in order to perceive the world is possible because of Receptive Fields. The idea of receptive fields, came about in the late 1800’s when scientists realized our retinas couldn’t have separate pigment genes for different colors that compared the colors in later stages of processing. This became clear when subjects were presented with a white screen after focusing on colored circles and the afterimage (or complementary color) appeared. If separate pathways were used for separate colors, the same color should be perceived on a white screen, not the inverse color.

If you were to make a cylinder by curling your fingers to touch your thumb and look through it, closing one eye, this is analogous to a single cells receptive field. Cones and Rods respond this way. When the correct stimulus enters that circle, the Rod or Cone will activate (for our purposes activation=1). If an incorrect stimulus (not the optimal wavelength) hits, the Rod or Cone will not activate (for our purposes, not activating=0).

Screen Shot 2013-03-04 at 12.52.01 PM

Now, imagine a smaller circle in the center of that big circle. This is analogous to the receptive field of a Bipolar Cell. A Bipolar cell gets inputs to the center of that circle from a single type of Rod or Cone, and gets input to the surround (the large encompassing circle minus the center circle) from a mix of differing types of Rods and/or Cones. Also, that center circle has a higher gain than the surround, meaning that instead of 1’s and 0’s, lets say 2’s activate the center, whereas the surround continues to activate to 1’s or 0’s.

The Red-Green Pathway

For example, if a  L ON/ M OFF Bipolar Cell is presented with circle of red light, it would activate maximally, but as green light starts to surround that red circle, the Bipolar Cell would begin to activate less and less, summing the center + inputs from the red and the – surround inputs from the green and firing respectively. At the same time, a neighboring M ON/ L OFF Bipolar Cell, would not fire at all to the initial red circle of light, for its receptive field would only be receiving – L (Red) inputs, but as the green light builds up in the  surround receptive field of the other Bipolar Cell, it encroaches on the center of the neighbor Bipolar Cells receptive field, subsequently adding +M, and initiating greater and greater firing.  This pathway is defined as the Red-Green Axis in Color-Opponency Theory. 

What about Blue?

Information from blue cones travels in a separate path to the 3rd stage of retinal processing (Ganglion Cells), but also joins with the information from Red and Green to create the Blue-Yellow Axis. Certain Bipolar Cells take information from a mix of Red and Green in the surround and from Blue in the center. The mix of Red + Green is defined as Yellow,and is subtracted by the center Blue (+2) responses.

Bringing it All Together

     These Different Bipolar Cells compare different inputs from different numbers and types of photoreceptors. Some Bipolar Cells (those in the fovea) get input from a single cone to it’s center, and from 10 or so cones to it’s surround. Others, in the periphery, get input from up to 5 cones in their center, and many more in their surround. Other helper cells (Horizontal and Amacrine Cells) help inhibit certain signals and certain times from certain photoreceptors to help enhance the reliability of the message passed along to Ganglion Cells.

      Where Bipolar’s mix and match these three optimal wavelengths (Red, Green, and Blue) at a local level (single Bipolar Cells) the differences in firing of each of the Bipolar Cells on a global level (the entire retina) is compared by Ganglion Cells. Ganglion’s then transmit this information to the brain for reconstruction of the visual world (Erikoz, 2010). From here, perception of shapes and hues in our visual scene finally begins.