Speaker 1: Welcome back, everybody. We're gonna be talking about sleep today,
and we'll also be looking at the neurobiology of sleep. Really,
that's kind of what we're going to be focusing on.
So sleep cycles through what they call nr EM stages
N one through N three, that's ends and nancy and
rem in ninety minute intervals. That's the way the cycle
happens for sleep. Some of the neurotransmitters and hormones involved
are serotonin, melotonin identity, and or rexin. They regulate sleep onset,
depth and timing. Insomnia has the most common sleep disorder.
Narcolepsy involves orxen deficiencies were you just fall asleep Everywhere
sleep disturbances worsen and maintain conditions like depression, anxiety, PTSD,
and bipolar disorder. I'll tell you sleep is one of
the biggest things that can help replying quite a bit.
They've even shown it drops one hour of extra sleep
can drop six to seven points on the Hamilton Depression Inventory.
It's pretty powerful stuff. Treating sleep problems biologically and behaviorally
improves the psychological outcomes of these people, of the people
with psychiatric issues, and for everybody. Really, it repairs tissues,
consolidates memory. When we get to memory soon, you'll see
how that operates. It recalibrates emotion and supports executive function
back there in the pre final cortex. So let's look
at some of a little bit more deep dive into
the ends. So each night, sleep repeats, as we mentioned,
a ninety minute cycle through non rapid eye movement. That's
what n RAM stands for, and RM is rapid eye movement.
So they just kind of abbreviate it to end one
and one is light sleep. But stage number one and
you transition kind of between wake and sleep. You got
different brain waves, and you're going to be in here
in the theta wave, so you have gamma and beta,
which usually your alert alpha, Theta and delta deltas are
completely out, so it's easily disrupted in the theta wave
and accounts for about five percent of total sleep. Is
a light sleep, the deeper light sleep stage n two.
You'll see on the EGS sleep spindles and k complexes
and temperature drops, heart rate slows. It makes up about
forty five to fifty five percent of your total sleep.
So I threw a couple of words in there. Sleep spindles,
which are brief bursts of high frequency brain activity. The
last about a half a second to two seconds. Again,
they're in stage two and they're linked to memory consolidation,
so sensory processing suppression as well and maintaining sleep stability
by blocking out external stimuli. The K complex is. These
are a sudden, sharp, high amplitude waves, often followed by
a slow wave lasting about a half half a second
to a second. They occur spontaneously in response to external
stimuli like noise. Their job is to protect sleep by
suppressing arousal while while assessing whether it's stimulus requires waking up,
but it's almost like your personal security. Both are hardmarks of
light sleep, aiding and transitioning to deeper sleep stages and
supporting cognitive functions like memory and learning. Now we go
to stage three, which is and three and this was
when you didn't get into the delta wave, so you're
pretty hard. You're knocked out. This is hard to wake from.
The stage is physically restorative. It supports immune function, growth,
hormone release, and memory consolidation. Unfortunately, it does decline with age,
so immune function here is why a lot of times
if you're not getting enough sleep, you're more susceptible to
getting sick. The fourth and final stage is what everybody
hears about rem sleep right. This is where you dream fast,
low voltage brainwaigh, but with muscle paralysis, which they call atonia.
Ato Nia is muscle paralysis. This stage is emotionally and
cognitively restorative, associated processing emotional memories, problem solving, and creativity.
We're not necessarily going to get into analyzing dreams here.
We will be doing that and some other podcasts that
I have. You can check those out at Circle of
Insight podcast or Psychology Tidbits. I have done some dream
analysis work over there. Now look at the newer chemistry
of the sleep wake cycles. They're regulated by homeostatic and
circadian processes. Think of them as pressure and timing. A
dentistine builds up during wakefulness. It's the body's sleep debt signal.
It promotes drowsiness and gets cleared during sleep, and then
it starts building back up. Cause Caffeine blocks the dentistine receptors,
which is why it keeps you alert. On a side note,
a lot of paramedics will use a dentistine to calm
down the patient at the time Melatonin is released by
the pineal gland, the pineal p I N E A
L and its response to diminishing light levels, So you
get both of these working together, a dentisine and melatonin
in a way. So when the light levels starts decreasing,
melatonin starts increasing in the pineal gland. At the same time.
Throughout the day, you're a dentisine is building up to
a certain level till you fall asleep, So both of
these are setting up your circadian timing. Note that exposure
to blue light from screens in the evening can suppress
melatonin release and disrupt sleep timing. Serotonin plays dual roles.
It helps initiate sleep and supports RAM regulation. SSRIs can
alter rem sleep patterns, often reducing RAM density. Orexin or
hypocretin orexin is ori E xi N producing the hypothalmus
keeps you awake and alert, and narcoleps orexin producing neurons
are deficient or absent, leading to sudden, uncontrollable sleep attacks.
Let's hurry over to your body's internal clock, which they
call the circadian rhythm. They're roughly twenty four hour cycles
regulated by the super chiasmatic nucleus the SCN in the hypothalmus.
The SCN responds to light input from the retina, sinking
the body clock to environmental cues like light meals social interaction.
When circadian rhythms are misaligned, think about overnight midnight shifts.
Things of that nature are jet lag, Sleep becomes fragmented,
and hormonal rhythms shift and mood regulation weakens. So look
now at some of the disorders associated with sleep. Will
also look at some treatment strategies. So insomnia disorder difficulty
falling asleep or staying asleep. Another one is early awakening
must last at least more than three nights per week
for three months and cause daytime impairment. The neurobiology associated
with it as heightened cortisol levels due to hyper arousal.
You also have an elevated metabolic rate and increase sympathetic activity.
Remember the fight or flight system kicks in here. First
line of treatment make sure you know this for the
exam is CBT. Also sleep hygiene, melotonin, short term sedative hypnotics,
and load dose trazodone. I've seen trousodon being prescribed a lot.
Also zopidim so. Again, first line of treatment is CBT
number two. It was obstructive sleep apney I repeated airway
collapse during sleep, causing brief arousals and oxygen desaturation. Often
missed unless the bed partner reports snoring or gasping. It
can lead to daytime fatigue, increase srutability that's also linked
to depression and hypertension. Treatment the most common is SEAPAP
weight loss, avoiding alcohol sedatives. By the way, SEAPAP is
the continuous positive airway pressure. It's a medical device that
they use to treat sleep. APNA delivers a steady stream
of air pressure through a mask worn over the nose
or mouth, keeping the airway open to prevent breathing in eruptions.
So what it does with the therapy can improve sleep architecture,
potentially increasing the frequency or quality of Stage two. This
is where we talked about sleep spindles and k complexes.
Better airway pagency reduces arousals, allowing more consistent sleep cycles.
We move on now to narcolepsy, which we've mentioned a
little bit earlier. Narcolepsy is characterized by sleep attacks, cataplexy,
sleep paralysis, and hypnagogic hallucinations. So you're hallucinating just before
you go to sleep. Cause is usually a resin deficiency
in the hypothalmus. Treatment is medophinol sodium oxybate structured naps.
Stimulants can work as well for alertness and SSRIs for
cattle AMPLEXI in cataplexy if you're wondering, is a sudden
brief loss of muscle tone triggered by strong emotions, either laughter, surprise,
or anger, often associated with narcolepsy. Episodes can range from
mild droopy eyelids to head nodding to severe full body
collapse lasting minutes I mean seconds to minutes, but preserved consciousness.
So again, sudden brief loss of muscle tone triggered by
strong emotions, and it is a symptom of narcolepsy. Sleep
in psychological disorder is depression, which we talked about earlier.
Shortened RIM latency, increased RIM density, poor sleep predicts onset
and relapse. Sleep disturbances are both a symptom and a
risk factor for depression. Unfortunately, antidepressants can suppress rem initially,
which may be therapeutic in the beginning. So I'm going
to take away that Unfortunately I mislooked at my notes.
Anxiety disorders difficulty initiating or maintaining sleep due to hyper arousal.
You got worry loops and elevated europe An effort to
disrupt pre sleep relaxation. Sleep deprivation increases a migular reactivity,
reducing emotional regulation as well. The increase in the megular reactivity,
of course, makes you hypervigilant. Third is PTSD also having
fragmented ram intrusive nightmares. REM rebound after trauma. Rem rebound
is a phenomenon where rapid eye movements sleep increases in
duration intensity following a period of rim deprivation or suppression,
such as from certain medications, stress, things of that nature.
It reflects the body's attempt to recover lost rem critical
for memory consolidation as we remember in cognitive function, so
rebound underscores the the brain's prioritization of rem sleep. In
addition to get nightmares maintain hypervigilance. For PTSD, prazosis in
an alpha one blocker can reduce trauma related nightmares, prosis
and p R A Z O s I N bipolar disorder.
Sleep deprivation can trigger manic episodes. Many of features decreased
need for sleep without fatigue sleep regularity is essential to
stabilizing mood cycles, so mood stabilizers often normalized sleep like valparate, depicoat,
or lithium. Lastly, it's a treatment strategy, so CBT is
your first line most effective long term treatment targets maladapted
beliefs and condition to arousal stimulus controls, sleep restriction, relaxation, training,
and cognitive restruction are some of the components. Pharmacological treatments
short term hypnotics so zopiderm, s zola, piclon, zopiclon which
is e z O p I c l O n
E which bind gabba, melatonin agonists like raalmaton which is
non sedating circadian regulators, ramaton is r ame te o
n E. Rexin antagonists like superoxytin that's s u v
O r e x A n T promotes sleep onset
without suppressing rem Antidepressants low dose trazodone common for insomnia
with comorbid depression or anxiety. And last is sleep hygiene.
Consistent schedule even on weekends, no screens or stimulating activities
sixty minutes before bed. I always recommend reading. I think
that helps a lot of tends to put people's kind
of get them drowsy just using out benergy in your
brain right soon much glucose, cool, dark, quiet environment and
no caffeine after two. Also avoid naff throughout the day
that are longer than twenty minutes. You don't want to
get into that mess for sure. We'll go back over
the importance of REM sleep, memory consolidation and learning, emotional regulation,
brain development, cognitive function, and neuronal restoration, so really important.
Also you'll see sleep there too. Remember REM rebound highlights
REM's importance. After deprivation, the brain prioritizes REM to recover
its benefits, often at the expense of other sleep stages.
This could alter into spindle and k complex frequency, but
underscores REM's role in the cognitive and emotional health of
an individual. So that's different. Now next time when we
come back, we move away from sleep and we're heading
into some of the foundations of human development across the
last span and how biology plays a role in human development.