Midterm III Comprehensive PDF

Midterm III Comprehensive Type Status Not started Lecture 14 : Sleep Deprivation IV: Brain Consequences - Memory, emotion & vodka shots Sleep deprivation & the brain: Pulling the all-nighter 💡...

Midterm III Comprehensive Type Status Not started Lecture 14 : Sleep Deprivation IV: Brain Consequences - Memory, emotion & vodka shots Sleep deprivation & the brain: Pulling the all-nighter 💡 sleep before learning is critical to forming new memories - without sleep, the brain regions that record new facts are shut down - e.g. hippocampus! As important as getting sleep after learning for memory retention. Development of Human Memories: Encoding → Consolidation → Recall. Research: Group 1 - 8 hours of sleep ; Group 2 - all-nighter → scan their brains when they were learning a new list of facts 40% decrease in learning abilities for the non-sleep group. + no sleep group showed less brain activity in hippocampus Sleep deprivation impairs the very region of the brain (hippocampus) dedicated to making new memories. Loss of sleep = loss of sleep spindles usually occurring in NREM and grow in stage 3 & 4 💡 Sleep spindles refresh the ability for new learning each and every night Sleep deprivation & the brain: The emotional brain without sleep 💡 sleep also appear to "reset" our emotional brain stability. and without sleep, our regulatory control over our deep emotional (amygdala) brain is lost → more reactivity! prefrontal cortex shut down + amygdala goes up! Midterm III Comprehensive 1  Amygdala - the emotional stability brain center = +60% activation when for the no sleep group Reason: amygdala, becomes overactive due to the inability of the PFC (which also gets shut down due to lack of sleep)- to controlling the amygdala as it normally does. Clinical Implications: Most psychiatric disorders (depression, anxiety, PTSD, schizophrenia, and suicide risk) have been found to be linked to sleep issues. eg. Peter Tripp. "The Boy Who Couldn't Sleep" - Chiari Malformation His brainstem couldn’t develop properly. This led to emotional instability and erratic behavior, demonstrating the close relationship between sleep, the brainstem, and emotions. Sleep deprivation & the brain: Alcohol, REM and losing memories 💡 dont even need total sleep deprivation, or even to stay awake to produce memory impairments e.g. alcohol can suppress REM sleep (last over 7 days!) and cause cognitive deficits long after learning has taken place! "complex cognitive test" → symbolic logic task (artificial grammar) three groups: 1)no alcohol, 2) alcohol during first night, 3) alcohol during night 3 regardless of day, if alcohol consumption impairments lasted up 7 days Midterm III Comprehensive 2  alcohol before bed, and not necessarily close to learning, prevents memories from being processing by sleep and retained.. even several nights later. impact of alcohol on REM: it fragments your sleep → you wake up more times its the metabolic byproduct of alcohol → once they've been broken down by your liver and kidneys, one of the thing that they produce are the aldehydes Aldehydes Strongly suppresses REM sleep, and therefore prevents these types of memory task (associative) from being retained Therefore, the loss of REM sleep, due to alcohol, prevented the retention of these memories - a process that continues after the first night to at least night 3 Weird dreams after drinking - REM sleep rebound effect: When the body misses REM sleep, it attempts to recover it later through a "rebound effect." This can lead to unusually vivid or strange dreams when waking up in the morning after drinking. Lecture 15 : Dreaming I - intro, emotional therapy & lucidity 💡 Dreaming happens across all sleep stages, but the likelihood and type of dream vary. —> most vivid, narrative, hallucinatory dreams com from REM sleep When do we dream? 1. NREM SWS : 0–20%. This is the deepest stage of sleep, and dreaming is less common here. If dreams occur, they are often less vivid and more thought-like. 2. REM Sleep: (here!) During REMs (eye movements): 95%. This is when vivid, story-like dreams happen. During non-REMs (no eye movements): 80–90% 3. NREM Stage 2: likelihood of dreaming. Dreams are still common Dream likelihood: 40–70%. here, but may be less vivid. This is a lighter stage of sleep, and while dreaming is less frequent than REM, it still happens. Dreams here might be less vivid and more fragmentary. Dreams are "psychotic": Hallucinations, delusions, Amnesia, disorientation, affective (emotional) liability Freud - The interpretation of Dreams Midterm III Comprehensive 3  💡 historically, the meaning of dreams has have ranged from messages/visitation from gods to the inner reflection of the soul, but Freud brought dream into the brain Sigmund Freud father of modern dream analysis and psychoanalysis Seminal "interpretation of dreams" was published in 1900 Proposed theory - disguised censorship, involving the discharge of repressed wishes Freud attempted to decode them, find the "psychic problem', and treat it Disguised Censorship Theory 💡 the dominate dream theory of 20th century (but no longer recognized as scientific) was Freud's model of Disguised Censorship - the masking of wishes/ desires (latent content i.e. meaning) to protect the sleeper, resulting in the manifest content( i.e. the dream itself) we have repressed wishes deep within the mind that are played out (discharged) when we dream, however they must come through a filter (censor → therefore its name of the theory), which disguises them, in order to avoid their expression in their "raw", obvious and undisguised form, which would cause the person to wake up. Freud claimed he had discovered the decryption code, with which he could reverse-engineer - interpret the dream - to solve underlying issues Problems with the Freudian Theory The problem with Freud’s theory is that it doesn’t have clear prediction or hypothesis. His theory is simply not testable (i.e. not falsifiable). It is both its brilliance and simultaneously downfall - science cant prove it right, but cant prove it wrong either! different analysts produce different interpretations of the same dream - suggesting subjectivity, lacking scientific objectivity. → took the same dream to different trained Freudian analytics, 3 completely different interpretations! → nothing replicable Beyond Dreaming - Lucidity 💡 Lucid dreaming ( when youare aware you are dreaming in sleep) is associated with electrical activity (40hz) re-emerging over the prefrontal cortex, and lucid dream acts (movement) can be observed using fMRI. Definition of lucidity- any reported activity upon awakening becoming aware that you are dreaming during the act of dreaming itself well practiced lucid dreamers can gain control over what and how they dream How can lucid dreamers tell you when they become lucid? Midterm III Comprehensive 4  come up with a predefined sort of language with the lucid dreamer through eye rolling! → measure with EMG channel eyes (muscles) are controlled by extra ocular muscles, and represent the only set of voluntary skeletal muscles that do not undergo paralysis! What changes in the brain during lucid dreaming? (EEG activity) during REM sleep and the dreaming state → lots of brain regions light up in their activity, movement regions, visual, emotional, and memory regions, they all burst into activity During wake, fast electrical brainwave activity is strong over the prefrontal cortex. During REM sleep WITHOUT lucid dreaming, fast electrical brainwave activity is absent, including over the prefrontal cortex. During lucid dreaming in REM, fast electrical brainwave activity re-emerges over the PFC, compared to non-lucid REM sleep dreaming, possibly explaining the voluntary control over the content of the dream But can we prove lucid dreaming with science? Took a group of lucid dreamers and did two separate fMRI scanning sessions while wake: instructed to clench left hand into a first over and over, then do the same right hand. Then, after entering REM and lucidity, they clench left and right hand into a first over and over, but IN THE DREAM showing similar brain areas activation! [LEFT PIC] while awake, left and right hand clench [RIGHT PIC] while lucid in REM sleep, a similar activated the opposite right and left sensorimotor pattern could be produced by the fictive dream cortex movements Midterm III Comprehensive 5  Lecture 16 : Dreaming II - Experimentally probing the dreaming brain Manipulating dreams - the failed history 💡 Early attempts at dream manipulation consistently failed to incorporate experimental "day residue" into reports. Many studies in the last 50 years (e.g. watch lights for hours, watching medical students to cutting up cadavers + cut dead body → They all failed!!) have tried to control what people dream about by experimentally controlling what they experience during the day: The theory was founded in Freud’s ideas of Day Residue : where something from the previous day makes it way into the dream content. The idea/goal was to manipulate this aspect in order to be able to manipulate dreams content. Sleep-onset, amnesiacs and video games Finally, using sleep onset (hypnagogic dreams), reliable stereotypes imagery can be produced by engaging, salient experiences (e.g. video games). 20 years ago: Used video games → subjects played 7 hours of Tetris over 3 days morning and evening sessions. The researches were trying to manipulate dream content in the hypnagogic dreams and understand part of the brain involved, which of those memory systems was actually controlling what carries over from waking life into dreaming life. 💡 Sleep onset dreaming → "hypnagogic dreams", transition between awake to sleep. People experience vivid sensory perceptions, such as sights, sounds, smells, tastes, and feelings of movement Group 1: novices (no prior experience) Group 3: Amnesic patients (temporal lobe brain damage - no hippocampus (initial memory inbox for fact-based Group 2: Experts (considerable experience) memories.) → e.g. epilepsy, cant make new memories Hypothesis: wanted to if the sleep onset dreams manipulated (game-play) was stored in the hippocampus → if stored in this region then Amnesic patients (missing this part of the brain) wouldn’t report the same results as either novices or experts. Experiment: every night across the three days, all patients would be woken up just as (they were falling asleep) → during the sleep onset hypnagogic period repetitively and prompted to report what were they experiencing. Results: Midterm III Comprehensive 6  Reports of Tetris imagery were similar across the groups, but interestingly only reporting facts about the game it self (shapes falling down and turning) not other aspects of experiments. Overall novices reported more than other groups proving that something unique and new is more likely to be a factor determining its presence in dreams from waking life. Amnesic patients also reported the effect more often than experts, further supporting it. Among amnestic patients: had no explicit memories of playing the game (or the study) yet they would instantly put their hands onto the keyboard. And on the same keys as if the procedure. Additionally, reported more than experts. Therefore, the memory must come from somewhere else in the brain, not the hippocampus. Overall: Importantly, note that none of the dream reports describe nothing like an episodic “replay” of the actual episode – i.e. no episodic memory reports of the experience. But instead, an abstraction, one that does not depend on the normal autobiographical reservoir of memory in the hippocampus The dreams are more about the distilled and most salient aspects of the game (the pieces) not the keyboard, the screen etc. Dreaming for overnight therapy: Theory: REM sleep and dreaming act as a form of overnight emotional therapy (also described as "emotional first aid"). Research Support: Studies confirm a critical role for REM sleep and dreaming in mental health, particularly in processing and regulating emotions. 💡 "emotional-memory"→ sleep to forget and sleep to remember: During sleep—especially REM sleep—the brain processes emotional memories in a unique way: Remember: The memory of the experience itself is preserved. Forget: The emotional charge surrounding the memory is stripped away in a "safe neurochemical environment." Mechanism : During REM sleep, the brain shuts down the stress-related neurochemical noradrenaline (associated with emotional and physiological stress), creating a calm environment without stress signals. This "safe neurochemical environment" allows the brain to process memories of emotional experiences without being overwhelmed by the stress associated with them. Essentially, your brain can "soften" the emotional intensity of the memory while keeping the factual details. Theory application: PTSD and REM Sleep: PTSD may result from the failure of the brain to strip emotion away from traumatic memories, potentially due to disrupted REM sleep. Repetitive Nightmares: A hallmark of PTSD, may result from the brain's inability to perform its "elegant trick" of detaching emotion from traumatic memories. why? Midterm III Comprehensive 7  When noradrenaline levels stay high or REM sleep is disrupted (like in PTSD), the brain can't effectively "strip away" the emotional charge from the memory. This is why traumatic memories in PTSD often feel as intense as when they first happened. Van der Helm et al. Current biology (2011) 💡 Key Finding: Incorporating sleep—particularly high-quality REM sleep—into emotional processing dissipates the strength of emotions tied to an experience. Prediction: The quality of REM sleep directly predicts the success of this overnight therapy, reducing the emotional impact of the experience. Study Design: Participants were split into two groups and underwent an emotional reactivity test using fMRI (recoding brain when showing pictures) about 9 hours apart: 1. No-sleep group: Tested twice on the same day—once in the morning and again at night—without sleeping in between. 2. Sleep group: Tested once at night, then allowed to sleep, and retested the next morning. Amygdala Activity: The study focused on the amygdala, a key brain region involved in generating negative emotional reactions. In the sleep group, amygdala reactivity was significantly reduced after sleep, showing that REM sleep helps dampen emotional responses. Sleep Benefit: The size of the emotional benefit (reduction in emotional reactivity) in the sleep group was positively correlated with both: The amount of REM sleep they experienced. The quality of REM sleep (referred to as "theatrical quality"). Lecture 18 : Sleep in the Clinic I: Insomnia insomnia is a common disorder (1:10 of population), defined by a difficulty falling asleep and/or a difficult stay asleep during the night. Diagnostic and Statistical Manual of Mental Disorders. (DSM-5) classifies Chronic “Insomnia Disorder” when: Dissatisfaction with sleep quantity or quality (e.g., difficulty falling asleep, staying sleep, early-morning awakening) Causes significant distress or daytime impairment Occurs at least 3 nights/week, for >3 months Two broad classifications/types of insomnia (can be combined) 1. Sleep onset insomnia: Difficulty falling asleep. 2. Sleep maintenance insomnia: Difficulty staying asleep or difficulty resuming sleep after waking up in the night/early morning. 3. **new aspect = "un-restorative sleep" Prevalence of insomnia in the general population (meta-analysis) shows: only ~10% of the general population is able to meet diagnostic criteria for insomnia. Yet, ~35% of the population have disturbed sleep once a week 💡 50% of patients under clinical care reported symptoms of sleep disruption → sleep problems seem to be perhaps one of the most common, either side effects or contributing factors to medical conditions Billy Crystal → "always thinking what do I need to do, what have i done" → creating stress response, flipping info & depression, rumination Midterm III Comprehensive 8  Biological changes 💡 Biologically, insomnia has been associated with changes in the body (e.g. cortisol) and changes in the brain during attempted sleep onset Normally, when falling asleep the brainstem should be normally powering off, which should shut down the thalamus, which should then prevent the cortex from sort of processing information within the brain. brainstem off → thalamus off → cortex not processing info Brain regions that do not "shut down" at sleep onset in insomnia patients vs. controls Excessive brain alertness activity Brainstem Excessive emotional activity Amygdala, Cingulate Excessive memory (re)activation. Hippocampus Overactive stress chemical in insomnia - Cortisol 💡 Cortisol : associated with fight or flight stress response that activates the NS. Study - drew blood samples every 30 min across a day (24hr). 2 IMP RESULTS: Most pronounced in the evening (sleep onset), and early morning (maintenance); Insomniacs had significantly elevated cortisol levels. 1. Thought the day insomnia patients present no differences in cortisol levels (high in the morning, and low in the night). But, just as approaching bedtime, instead of decreasing cortisol levels start rising again. = (showing the difficult to fall asleep category) Midterm III Comprehensive 9  2. Also, in the middle of the night, when cortisol levels should be rising gradually in normal people, for insomnia patients they start rising more than they should. (diff to stay asleep) These two abnormal spikes in cortisol of the fight or flight system (right at bedtime & in the middle of the night) fit very well with these two symptom profile's → Can't fall asleep or can't stay asleep. Confirms the idea of insomnia in a way or impart is related to excessive stress related activity Treatment of insomnia 💡 Pharmacological treatments (sedative hypnotic drugs, that is, sleeping pills) have limited benefits in the short term for certain types of insomnia and have problematic side effects and safety concerns Medications → GABA receptor targeting drugs (e.g. Ambien, Sonata, Valium) GABA is the main inhibitory neurotransmitter of the brain. Sleeping pills, know as “sedative hypnotics”, target GABA receptors → i.e., they sedate the brain. They don’t produce natural sleep. SEDATION ≠ SLEEP! Also, side effects: daytime drowsiness ("drug hangover"), insomnia rebound when discontinued Memory problems → including unremembered nighttime activities → e.g. 4am call Tolerance (need to keep increasing dose for same effect) → need to increase intake to keep up the "clinical benefits" → the more intake, more side effectives Extra Studies (associational not correlation = therefore, do not establish direct causality) Several large-scale epidemiological studies showed concerning results, linking use of sedative hypnotics to risk of premature death and cancer. Behavioral therapy - safer & more effective solution → CBT-I (now recommended 1st): CBT-I: main objective of is to alter those factors that perpetuate or exacerbate sleep disturbances. Working with a therapist to develop a personalized sleep strategy and restore confidence: You control your sleep, not the other way around. Learn skill. Provides similar results to sedatives in the short term but better in long-term, 20% more effective even clients disengage from the therapist with CBT-I compared to Ambien. Lecture 19 : Sleep in the Clinic II: Narcolepsy 💡 Narcolepsy: is a chronic neurological (long-lasting) disorder affecting over 1/4 million Americans (similarly to Multiple Sclerosis). A majority of people go their whole life without even knowing they have this disorder. Prevalence & First Signs Narcolepsy is exemplified by extreme sleepiness/tiredness during the waking day. Onset can occur any time, but usually between age 10-20. Narcolepsy does not appear to run in families i.e. is not genetically inherited, but does appear to be related to a genetic mutation. Yet, genetics alone don’t fully explain the prevalence. Symptoms & Manifestation Four key symptoms of Narcolepsy: 1. Excessive Daytime sleepiness (EDS) a. Daytime sleep attacks. The sleepiness a patient feels is about the same as staying awake for 3-4 days straight. b. Overwhelming, irresistible drive to sleep at times when you want to be awake. c. First symptom to appear, and often the most troubling. Midterm III Comprehensive 10  2. Sleep paralysis (REM related - out) a. Temporary inability to talk/move when falling asleep or waking up. b. Usually occurs during the transition out of REM – brain is partially asleep, partially awake – paralysis still in place. i. Sleep paralysis is not unique to narcolepsy ~25% of population have experienced it (i.e., as common as hiccups) c. Often associated with feelings of dread and of intruders present. d. Believed to explain the vast majority of “alien abduction” claims. 3. Hypnagogic Hallucinations (REM related - in) a. Vivid and often scary dreams and sounds reported when falling asleep. b. These episodes often coincide with REM sleep onset (atypical), commonly accompanied with sleep paralysis as well. 4. Cataplexy ~ "kata" = down + "plexis" = seizure a. Sudden loss of muscle control ranging from slight weakness (head droop, facial sagging, jaw drop, slurred speech, buckling of knees) to total collapse. b. Cataplexy is not sleep but WAKE - essentially this is REM paralysis without the REM. c. It is commonly triggered by intense emotion (laughter, pleasure, anger, surprise, fear) or strenuous athletic activity. d. Most persons with narcolepsy have some degree of cataplexy. Cause, Mechanism & treatment→ loss of orexin = unstable control switch 💡 while the true cause remains unknown, it appears a loss of orexin releasing brain cells may contributes, resulting in an unstable wake-sleep control switch of brainstem activation Three critical brainstem centers that active the brain and keep us awake: Acetylcholine (ACh), Noradreanaline (NA), Serotonin (5-HT) They activate the thalamus (sensory gate) and cortex, making us alert But what switches them on → Orexin! 💡 Orexin is a neurochemical, released from the hypothalamus, which stimulates the 3 brainstem centers (ACh), (NA), (5-HT). When it does, these brainstem centers turn on and activate the thalamus and cortex. Thus, Orexin acts like a light switch, turning the brainstem ON! When Orexin is NOT released, the 3 activating brainstem centers are not stimulated. They consequently turn off and the brain becomes deactivated → Thus, without Orexin the switch for the brainstem is turned OFF! Midterm III Comprehensive 11  Narcolepsy is associated with a significant loss of Orexin brain cells. Adding to the problem, there also appears to be a reduction in the number of Orexin receptors (receiving sites) in the brain. Because of this lack of Orexin (release and reception), the narcoleptic brain is like an unstable switch hovering in the middle point of wake/sleep Normally, Orexin is released during the day, keeping the brainstem switched ON, hence keeping us awake. 💡 In narcolepsy, due to the lack of Orexin, the brainstem switch is stuck between ON and OFF, resulting in unstable set point between wake and sleep. Treatment (only for 1 & 4 → EDS and Cataplexy) 💡 Treatment possibilities are limited, with wake stimulating drugs used to override the broken switch, and anti- depressant to reduce cataplexy (reduce REM) 1. Excessive Daytime sleepiness (EDS): Originally, stimulants such as amphetamines (horrible side-effects). More recent stimulating drugs e.g. Provigil/Modafinil→ awake promoting stimulant. Doesn't prevent condition, but reduce frequency & severity 4. Cataplexy: Anti-depressant appear to reduce the amount of cataplectic attacks: (possibly works because they inhibit REM sleep) → Cataplexy belongs to the REM sleep paralysis mechanism 💡 2. & 3. → NONE treatment for sleep paralysis and Hypnagogic Hallucinations Lecture 20 : Sleep in the Clinic III to IV: Parasomnias, REM Behavioral Disorder & Fatal Familial Insomnia Parasomnias: Types, cause & a case of homicidal somnambulism “para” beside/at the side of “somnus” sleep (Roman God of). Includes: Midterm III Comprehensive 12  (from SWS): Sleepwalking, Sleeptalking, Sleepeating, Sleeptexting, Teeth grinding, Night terrors, Restless legs syndrome from REM: REM behavioral disorder* Often more common in children decrease with age → this is probably related to them having more SWS as one of the explanations Associated with with stress and depression in adults → can be triggers Causes & triggers Caused by inappropriate activation of the “fight or flight” nervous system. This ‘jolt’ of nervous system activity results in an sharp ejection from SWS, where the brain attempts to wake up. 💡 But the brain gets “stuck” in- between the sleep-wake states Activity in the brain What changes in the brain when the patient has a burst of fight/flight nervous system activity in the body? A PET scanning study in a single individual showed that sleepwalking associated with: Increased activity of the motor systems → Primary motor cortex Decreased activity of conscious-based logical control center PFC 💡 going into automatic mode that aren't thinking about what they're doing, they're just doing. (low PFC and high motor cortex activity) Homicidal somnambulism - Kenneth James sparks (Broughton et. al.) 23-year-old Toronto man with insomnia from joblessness and gambling debts. Had extensive history of parasomnias: nearly sleepwalked out a window at age 11, was a deep sleeper, and had strong family history of various sleep disorders. While sleepwalking, drove to in-laws' home, killed mother-in-law, injured father-in-law. Even if not having a personal motive. Turned himself in to police, unaware of his actions until seeing his injured hands. Found not guilty in 1988 due to sleepwalking defense. Similar defenses rarely succeeded in later cases Three key (precipitating) factors preceded the incident: 48 hours of sleep deprivation Physical exhaustion from rugby Emotional stress from gambling debts. 💡 * sleep walkers should avoid the precipitating factors in terms of sleep deprivation, physical stress, and deal with their emotional stress the best way possible. REM Behavioral Disorder: Symptoms, features and cause In REM sleep behavioral disorder (RBD), the mechanism that causes muscle paralysis during sleep begins to fail. This means people continue dreaming but without the usual paralysis. Loss of normal muscle paralysis during REM sleep → act out dreams, often violent in nature. Dream-enacting behaviors include: talking, yelling, punching, kicking, sitting, jumping from bed, arm flailing, and grabbing. Has also been associated with non-volitional homicide. Appears to be caused by dysfunctional brainstem REM mechanisms that normally controls REM paralysis. → When the brainstem activates during REM sleep and activates the cortex, there's another signal that's sent down Midterm III Comprehensive 13  the brain and into the spinal cord, paralyzing all of the alpha motor neurons and voluntary skeletal muscles. In RBD, this mechanism within the brainstem degrades. Almost 80% of those with RBD are men. RBD is also a strong predictor of Parkinson's disease, 1/3 developing Parkinson's. This can occur up to 20 years before other Parkinson's symptoms appear. Treatment clonazepam → ~ 90% effective in decreasing the symptomatology that the likelihood of this happening. Antidepressant → decrease among of REM sleep Animals exhibit REM Sleep behavioral disorders too Fatal Familial Insomnia: Description, mechanisms and example FFI - During normal wakefulness, the brainstem—the brain's power station—fires up and stimulates the thalamus. This opens the thalamus for sensory input, like a door or awareness switch. All incoming signals flow up to the cortex, where the information is processed. This allows us to be awake & aware of the outside world, consciously processing our environment. 💡 awake: Brainstem (fires up) → Thalamus opens → sensory systems sent to cortex to be processed During normal non-REM sleep, the brainstem shuts down, which stops stimulating the thalamus. Without this stimulation, the sensory gate of the thalamus closes. As a result, signals from the outside world can no longer reach the cortex through the thalamus. The cortex then drifts off into sleep, and we cycle through the stages of non-REM and REM sleep. 💡 Brainstem turns off electrical brain power → Gate is closed, thus information cannot enter brain further → Information sent to the cortex = fall asleep What does this have to do with fatal familial insomnia? prion protein many prion diseases → fatal familial insomnia, mad cow disease etc. these proteins that are naturally occurring within the brain change the structure. And when they change their structure. They become problematic and they start damaging specific parts of the brain. Now here in fatal familial insomnia, those prion proteins start to attack the thalamus. Now they do attack other areas, but they degrade and attack the thalamus very significantly. "eating away at the thalamus" → the thalamus can't operate normally → it can't be closed shut, at least not fully. the gate remains partially open. In other words, the brain can never shut itself off because it can never close. → Because these prion proteins have attacked the thalamus. Result in - there's always information going up to the cortex. The patient can never shut off. The patient can never fall asleep Treatment: n/a trying to educate your family, further consider if they wanna have children summary Parasomnias are disorders occuring from or during sleep, including sleepwalking, sleeptalking, sleeping eating, night terrors sleep walking occurs from deep NREM sleep (SWS), caused by an abrupt awakening attempt by the brain while most "episodes" are short and non-violent, this is not always the case RBD represents a different type of disorder, reflecting the abnormal loss of normal REM atonia, resulting in the acting out(often violently) of dreams Fetal familial insomnia is a genetically inherited disease, causing degeneration of the thalamus and offer increasing evidence a lack of sleep is leathal Midterm III Comprehensive 14  Discussion (Dreams + Parasomnias) Discussion #8 Dreams What Counts as a "Dream"? Dreams can pull from: Episodic memory sources: Elements of real-life experiences (TV-episodes) Full episodic memories: Rare (1-2%) complete replays of past events. (rational) How Dreams Are Studied: Researchers use the following methods to study dreaming: Meta-analysis Study: A study tested how often people recall dreams by waking them during different sleep stages and categorizing their responses. Patterns observed: Stage Dream Type As sleep progresses dreams content Real-life memories (episodic memory sources) + logical Sleep Onset becomes more thinking (directed thinking). distanced from real NREM Sleep Fewer real-life memories, less logical thinking. life to bizarre in REM Sleep Wild, creative, and emotional dreams (hallucination-like). REM Dream-lag Effect: A delay (typically a few days) between experiencing something (e.g., an emotional or memorable event) and it showing up in your dreams. Study: Participants watched a distressing film (e.g., buffalo sacrifice). then Researchers collected dream reports from participants over the following week and rated how strongly the dreams were linked to the movie. Participants with strong initial links to the film in their dreams showed a delayed peak in related dream content a few days later Participants with weaker or no initial links to the film had no significant delayed peak. Delayed Incorporations: Dreams after a few days were more likely to involve: Interpersonal relationships (connections between people), Resolved problems (solutions or emotional processing), Positive emotions, Spatial locations (places seen in the film). 💡 Results: The dream-lag effect shows that dreams rely on different brain regions (hippocampus and neocortex) at different stages of memory processing. Early dreams reflect raw memory details, while later dreams reflect integrated, emotional, or abstract versions of those memories. Brain Region Role in Memory Consolidation Dream Content Active initially (short-term memory Early dreams tied to raw, factual Hippocampus formation); decreases with time. memory details. Gains activity over time (long-term Later dreams are more abstract, Neocortex memory storage). relational, and emotionally processed. 💡 Possible Explanation: Memory consolidation: The brain processes and reorganizes memories over time. The hippocampus is initially involved in forming new memories but becomes less active as memories are stored elsewhere in the brain Midterm III Comprehensive 15  Key Idea: Dream Content Changes Over Time: Early dreams: Closely tied to the hippocampus, focusing on raw details of the memory. Later dreams: Processed by the neocortex, focusing on emotions, relationships, and integration with other memories. Stress and bad dreams Prevalence: Most adults have at least one nightmare per year. Nightmare rates are higher in younger adults, starting around age 14. 💡 Strong link between nightmares and waking psychological stress. Study: Effects of the 1989 Bay Area Earthquake on Nightmares Stressful events (like an earthquake) can double the frequency of nightmares, especially for people closer to the event. The farther people are from the source of stress, the fewer nightmares they report. This highlights how external stress impacts our dreams. Discussion #9 Parasomnias 💡 NREM parasomnias: Mainly disorders of arousal, usually occur during SWS, decrease with age 1. Confusional arousals 3. Sleep walking 2. Sleep terrors 4. Sleep Eating, Sleep Texting, Sleep Sex Triggers: fevers, alcohol, physical activity, stress, medications, previous sleep deprivation The delta frequency persists following arousal for several seconds → such patterns can be seen in confusional arousal or sleep walking episodes arising from SWS Confusional arousals: Acting in a strange or confused way upon awakening, usually from SWS Symptoms can include: slow speech, confused thinking, poor memory, blunted responses to questions/ requests, thrashing (in children), inconsolable crying (in children), automatic behaviors (fairly harmless), sleep drunkenness Sleep walking: Involves various complex motor behaviors (eg. walking) initiated during SWS most common in children (1-17%), under-acknowledged in adults motor activity can vary in complexity and duration, little to no memory of the incident Sleep terrors: In adults, sleep terrors can occur when sleep is fragmented by other sleeping problems. Obstructive sleep apnea (OSA) is a common medical problem that can lead to frequent arousals from sleep. initiated by screaming, Characterized by panic, running, or other movements Sleeper is often inconsolable, Complete/partial amnesia Most common in children Treatments: reassurance, behavioral therapy, and medication Sleep-related eating disorder: usually occurs during NREM sleep in the first half of the night and is associated with the transition from NREM to arousal during sleep. Midterm III Comprehensive 16  Frequent episodes, generally nightly, of eating and drinking in an out-of-control manner Impaired consciousness while preparing and eating food & Little memory of these actions Eating high-carbohydrate and high-fat foods or odd combinations of food: sometimes inedible or toxic substances Possibly experiencing injuries or engaging in dangerous food preparation activities Sleep texting Study - texting and phone use during sleep. Objective: To examine the influence of cell phones and sleep quality among college students and the prevalence of sleep texting. Methods: A survey was used to ask about cell phone use during sleep and sleep quality. Students were asked about hours of sleep, both on a school night, and over the weekend in addition to location of cell phone. Results: A quarter of the sample (25.6%) reported sleep texting behavior along with poor sleep quality and the cell phone influencing their sleep. Students that sleep text were more likely to report sleep interruption, when placing the phone in bed with them. have no memory of texting (72%) or what they texted (25%). Conclusions: Sleep texting and its influence on poor sleep habits is a growing trend in a college student population. Sexsomnia (SBS): is when an individual will moan from arousal, masturbate, or try to have sex while completely asleep. The person almost always has no control over their actions and no memory upon waking. While there is no known cause, there are possible triggers including stress, fatigue, and controlled substances. Individuals who engage in sleep sex do things of a sexual nature in their sleep and later have no memory of their actions. Sexsomniacs are often grouped into three different categories based on their actions during their sleep Vocalization: those who moan while asleep and pose no real direct threat to their bed partner. Masturbation: those who masturbate while asleep and can cause themselves and their bed partners injury if they are too aggressive or try to involve their partner in the act. Intercourse: those who attempt to have sex during sleep with their sleeping bed partner or someone else - often resulting in injury to themselves or their unwilling partner. Midterm III Comprehensive 17