Psychology

Sleep Paralysis: Conscious Yet Frozen

You are in your bed after a long day, about to fall asleep. You finish reading your book, scrolling on your phone, sending an email, and hit the hay. Then, you wake up the next day in your bed. You might have been dreaming about frolicking in a field, cleaning your house (I hope not), going on vacation, or a variety of other things. But… you wake up in your bed. Not in a different country, not in a different area outside of your home, not even in a different room in your home. You wake up in the exact same place where you went to sleep: your bed. How is this possible?

Sleep paralysis is a deeply researched phenomenon in which, during sleep, you are unconscious and yet unable to move (prompting the apt name). Now, you can still curl your toes, flex your hands, or twist and turn, but you can’t actually get out of your bed and say, clean your house (provided you don’t have night terrors or some other conflicting sleep disorder). But how does sleep paralysis occur? Why can’t we just do our chores when we are dreaming, or rather dreading, them the next day? 

Our brain is considered to be one of the most complex objects there is. From being able to have half of it removed and still function just about perfectly (in another phenomenon referred to as plasticity, or the brain’s ability to repair itself), to being able to not feel pain and yet regulate pain for all the other parts of the body, it’s a pretty unique and powerful organ. Millions of neurons and hundreds of parts within it work to make it function as it does, all without making us sweat even a little. But there are three particular things that explain sleep paralysis: the brain stem, the motor cortex, and movement signals. 

The motor cortex is responsible for initiating your movements. Whether it’d be raising your arms to stretch, climbing a step with your legs, or even scrolling on your phone, you can thank your motor cortex. In all of these actions, the motor cortex sends movement signals to your brain in order to actually cause you to, well, move. During sleep, although you are not conscious, your brain still is active (as it doesn’t ever ‘shut off’). The body acknowledges this and programs your brain stem to block all movement signals from the motor cortex in an effort to protect you by preventing you from wandering off and, say, doing some chores. 

You might be wondering why you can still curl your toes, toss and turn, or even move away from something unpleasurable. After all, the motor cortex is responsible for movement, no? Well, that’s true to an extent: it’s responsible for all voluntary movement, that is. Remember your last doctor’s appointment where they used the tiny rubber hammer to test your knee’s reflexes? That wasn’t voluntary, so instead of going up to the brain, it is only sent to the spinal cord, which the brain stem does not block movement signals from. As such, all reflexes (and certain small movements) are permissible by the brain because, well, they don’t actually go through it.

The brain is an intricate thing. It’s responsible for every single facet of your life, and yet does its job so seamlessly that we hardly even think about it. It even protects us at night when we are sleeping. What else can the brain do that we haven’t discovered? What else does the brain do that we marvel about? 

Sources

  1. https://www.sleepfoundation.org/parasomnias/sleep-paralysis
  2. https://my.clevelandclinic.org/health/diseases/21974-sleep-paralysis
  3. https://sleepdoctor.com/parasomnias/sleep-paralysis/

Unraveling the Enigma of SSRIs: How Do They Work, and Do They Really?

Image from: https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.verywellmind.com%2Flist-of-ssris-380594&psig=AOvVaw0XM6qzBGJgJ5sqoor-jvoP&ust=1697051716630000&source 

SSRIS, or Selective Serotonin Reuptake Inhibitors, are a type of psychiatric drugs used to treat symptoms of depression and anxiety, or depressive and anxiety disorders. They are the most commonly prescribed antidepressants, and first began being used clinically in the late 1980s. The first ever SSRI, fluoxetine, was cleared for prescription usage in the United States in 1988, and paved the way for a new, much more reliable form of antidepressants. As of 2018, it is estimated that 13.2% of Americans above the age of 12 are on some form of SSRIS. The question is, what are they, really, and how do they work? 

It’s important to first understand the Serotonin Hypothesis of Depression. This hypothesis states that low levels of serotonin (a neurotransmitter related to mood, sleep, digestion, and much more) in the brain, or an inability to process serotonin correctly, is the leading cause of depression. Within this hypothesis lays the groundwork for SSRIS; the theory being that increasing serotonin in the brain lowers symptoms of depression. Therewithal, it is incredibly difficult for scientists to measure serotonin levels, as when done through bodily fluids, such as blood, urine, or cerebrospinal fluid, deficits do not appear, even when the person has been clearly diagnosed with depression. This is because neurotransmitter levels in the brain are extremely localized, and therefore not well reflected by levels throughout the rest of the body. This makes it difficult for scientists to objectively ‘prove’ the serotonin hypothesis, and as of 2022, many psychiatrists no longer accept the serotonin hypothesis, claiming there is no direct correlation between serotonin levels and depression. But, if the serotonin hypothesis is false, why are SSRIS so commonly used, and do they really work? 

Here’s what we do know. After a few doses of an SSRI, serotonin levels in the brain increase. This happens because the SSRI blocks the reabsorption (or reuptake) of serotonin into the neurons, allowing the neurotransmitter to better send messages between neurons. SSRIS are classified as selective because they only block the reabsorption of serotonin, and not of other neurotransmitters. If the SSRI works properly, the patient should see decreased symptoms of depression within the first two weeks to a month. And that’s it. That’s how they work. It seems quite simple, and foolproof, but many psychologists have begun to find holes in the argument for this. 

Research done by Moncrieff et al includes compelling data suggesting that there is no consistent evidence linking lowered serotonin concentration or activity to depression. They therefore suggest it is “time to acknowledge the serotonin theory of depression is not empirically substantiated.” This leads many to question the effectiveness of SSRIS. But how could that be? For the most part, patients who use SSRIS report their symptoms of depression and anxiety decreasing significantly, as well as their mood stabilizing. It is possible that this is partially because of a placebo effect, which is when a person’s belief in the treatments is what is causing their improvement, and not the treatment itself. It is also possible that researchers claims do not hold as much truth as they believe. Despite there clearly being evidence of a lack of a correlation, there is also decades worth of evidence that SSRIS do work. 

Image from: https://www.google.com/url?sa=i&url=https%3A%2F%2Fhopes.stanford.edu%2Fssris%2 

Furthermore, it is important to note that we do not understand everything about SSRIS. The brain, and therefore, psychiatric medications, are incredibly complex. We tend to find that there isn’t just one answer to the psychology questions we seek, especially when considering that everyone is different, and there are lots of things we still don’t know about the brain. Psychiatrists and psychologists alike do not suggest stopping SSRIS if you are on one, especially not without consulting your physician. As research continues, we hope to find more of the answers we seek, although it’s hard to say what the near future holds for current theories about SSRIS and other psychiatric medications. 

Sources: 

https://www.mayoclinic.org/diseases-conditions/depression/in-depth/ssris/art-20044825

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9669646/#B17

https://www.psychologytoday.com/us/blog/denying-the-grave/202209/we-still-don-t-know-how-antidepressants-work

https://www.nhsinform.scot/tests-and-treatments/medicines-and-medical-aids/types-of-medicine/selective-serotonin-reuptake-inhibitors-ssris#:~:text=It’s%20 thought%20to%20have%20a,messages%20between%20 nearby%20never%20 cells.

https://www.cdc.gov/nchs/products/databriefs/db377.htm

Déjà Vu: The Brain’s Mysterious Illusion

We all know what déjà vu is, and no, we’re not talking about Olivia Rodrigo’s hit song. But what does it mean? A reported 97% of people have experienced déjà vu, but most don’t understand what it truly is. So, what psychological processes are involved in that odd, reminiscent feeling? Why does it happen? Why are our brains tricking us? Is it dangerous? Read to find out!

Technically, déjà vu is your brain creating an illusion. According to the Cleveland Clinic, déjà vu is caused by a dysfunctional connection between two parts of your brain. As explained by Dr. Khoury, a Neurologist and MD, déjà vu is a “subjectively inappropriate impression of familiarity of a present experience with an undefined past.” Basically, you feel you’re re-experiencing something you are almost sure you couldn’t. Scientists have traced this phenomenon back to recognition memory, composed of two aspects: recollection and familiarity. The hippocampus and prefrontal cortex control these aspects, respectively. The hippocampus controls long-term memory formation and spatial memory, allowing us to identify the position of objects regarding our bodies and concerning other objects. This contributes to the hippocampus’s ability to control recollection. Recollection allows us to remember and recognize things we have experienced before and to recall information (like on a test). Furthermore, the prefrontal cortex, specifically the lateral regions, including the anterior and dorsolateral prefrontal cortex, are responsible for familiarity. Familiarity memory occurs when a situation feels familiar, but a specific memory cannot be pinpointed. 

When your brain confuses a familiar memory for that of a recollection, déjà vu occurs. This creates the emotional sensation of an inscrutable memory. Because your brain interprets said familiar memory as recollective, you feel you’re sure you’ve experienced the memory before. Still, the brain’s inability to locate the memory (seeing as there isn’t truly one) complicates things, making the memory seem hazy and almost like a dream. This produces the confusion of knowing there’s no way you could have experienced the memory in the first place. 

What is Déjà Vu?! - YouTube

Image source: PBS, https://m.youtube.com/watch?v=ut8mYGi0YRs 

For the most part, déjà vu is an entirely normal and healthy reminder that our brain isn’t perfect and makes mistakes, just like us. In rare cases, déjà vu can indicate a neurological disorder. As a possible effect of temporal lobe seizures, many individuals with epilepsy report frequent feelings of déjà vu. Epilepsy often includes focal seizures that occur in the brain, and it’s possible to have said seizures in the frontal and temporal lobes, where the prefrontal cortex and hippocampus are stored, respectively. These seizures are generated by uncontrolled electrical activity that causes nerve cells to misfire in the brain. However, don’t worry if you just experience déjà vu occasionally. Focal seizures frequently have a slew of other signs, such as lack of muscle control, twitching, having sensations involved with all five senses, confusion regarding where you are, and frequent, sudden, unexplained emotions (so there is no need to call up your doctor and ask if you have epilepsy, simply because you’ve experienced déjà vu). If you do ever feel like you are about to have a seizure, it is important to notify someone immediately and contact a doctor if the issue persists. 

Sources