While you were sleeping (WYWS) Final study guide

Process S

"S" stands for Sleep Pressure or Sleep Debt

Homeostatic (constant, stable)

Sleep propensity increases the longer you stay awake

Sleep propensity decreases with sleep

You can think of Process S as intensity of sleepiness or a drive to put you to sleep

Process S is homeostatic

Growth hormone and Plasma Prolactin is under process S

Process S is sleep debt

Process C

"C" stands for circadian

A self- sustained biological rhythm normally synchronized to roughly 24 hours

Circa means "approximately" or "near to"

Dia means "day"

the site of Process C is Suprachiasmatic nucleus (SCN)

Process C is: strongest at the end of the day, related to body temperature

Process C is circadian rhythm

Opponent Process (Two Process) Model

Delta power or SWS during NREM can be used to estimate Process S

Delta power increases logarithmically as waking is prolonged

Core Body temperature is often used as a measure of Process C

Sleep propensity is greatest during the falling limb of the circadian body temp rhythm and decreases on the rising limb

Human and animal studies suggest that process C regulates arousal and REM but that NREM M is more strongly under the control of Process S

Suprachiasmatic nucleus and zeitgebers

where the clock is

Suprachiasmatic nucleus (SCN)

Located at the optic chiasm, where the optic chiasm, where the optic nerves cross, within the hypothalamus

Keeps the body on a roughly 24-hour clock but not perfectly and so still requires environmental cues (zeitgebers) to calibrate daily

Zeitgebers: Time Givers

Influences on timing of the circadian pacemaker

The period of the circadian pacemaker is not exactly 24 hours; organisms rely on external time cues to align their circadian system with the environment (entertainment).

"Zeitgebers" are "time-givers" and remind our bodies of what phase (awake/asleep) we should be at within a given environment.

In order of strength:

Light (most powerful)

Meals

Exercise

Caffeine

Larks and Owls

Humans probably evolved to sleep as groups and families, not couples

Larks- go to bed early and awaken early to guard the clan

Go to bed at 9pm, awaken at 5am

Owls- stay up late to guard the clan

Go to bed at 1am, awaken at 9am

Sleep patterns (phase differences) in circadian rhythm disorders

Melatonin (function, site of origin)

A naturally occurring hormone found in animals, plants and microbes

Synthesized from tryptophan

Secreted into the blood by the pineal gland

Also found in high concentrations in bone marrow, lymphocytes, and epithelial cells (not regulated by the photoperiod in these cells)

Secreted in darkness

Inhibits secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from anterior pituitary gland

Kisspeptin

A protein that signals GnRH (gonadotropin releasing hormone) to start puberty

Kisspeptin is inhibited by melatonin

Children living on or near the equator see more sunlight, release less melatonin, and experience earlier puberty

Causes mild drowsiness and lowers core body temperature

Melatonin signals the start of sleep but isn't highly soporific

Production by the pineal gland is inhibited by light to the retina and permitted by darkness

Blue light (460-480 nm) suppresses melatonin

Wearing glasses that block blue light in the hours before bedtime may prevent melatonin loss (and help to adjust to an earlier bedtime, e.g., advance the clock)

Also has a role as an antioxidant,

Melatonin is high during the night and low during the day when under constant dim light conditions.

Melatonin with Age

Production of melatonin decreases with age

Adult melatonin production begins around 6-8 PM and peaks until 4 AM, stopping production around 5 AM

Adolescent melatonin production begins around 11 PM and peaks until 7 AM, stopping around 8 AM

Explains the adolescent delayed sleep phase, relative to adults

So waking an adolescent at 7 AM is like waking an adult at 4 AM

Jet lag

Hour a day, you want to keep to your home schedule +/- 1 hours each day

What we try to do: adjust your clock by about an hour a day

With light, caffeine, melatonin, and time givers

Trick your brain into thinking you are in between time (advance 2 hours ahead instead of 6)

Put your sunglasses/blue light glasses when you don't want light

Jet lag

Effects on the body

Generally transient and include:

Difficulty sleeping

Excessive daytime sleepiness

General malaise

Impaited performance

Gastrointestinal upset

Usually influence by direction of travel:

Slower adaptation when traveling east

Increases with the number of times zones crossed

Generally: people do better traveling west

Eastward Travel

The sleep cycle is shifted ahead (e.g., it's earlier where you arrive) or advanced

Usually, people sleep well the first night in the new locale (especially if they stay awake the day of arrival and sleep at the new locale's usual bedtime)

Probably due to Process S and a large sleep debt that accumulates, despite a misaligned Process C

Marked increase in stage 2 sleep on first night in new time zone; compensatory increase in REM several nights later

By the second night, however, Process S is less influential because much of the excess

Westward Travel

Changes in sleep quality after a phase delaying westward flight lasts fewer days for most people

Westward travelers show and increase in slow wave activity on the first night in the new time zone (showing an increase in sleep pressure, like eastward travelers)

This makes sense because most westward travelers stay awake during the flight and then stay awake until the usual new destination bedtime, so they've accumulated more sleep pressure Over the next few days, people often fall asleep easily but have late insomnia(early

East vs. west

In general, following phase changing travel, there is little trouble falling asleep the first night upon arrival because of an increase in sleep pressure (process S)

East

Usually people have more difficulty initiating sleep following eastward travel (a few days to a week) because they've been advanced

West

More difficulty maintaining sleep later

Core body temp

There is a small window related to the endogenous body temperature rhythm (as it approaches its daily minimum) during which time we may fall asleep and maintain sleep throughout the night

Misaligning CBT minimum with the light/dark cycle is a major target for jet lag desynchrony

Adjusting this, starts to drop an hour before habitual bedtime, we loose 1.8 degrees Fahrenheit on average

Role of bright light and melatonin

AM

Light advances the clock

Melatonin delays the clock

PM

Light delays the clock

Melatonin advances the clock

Light exposure during the Lag traveler's biological night (as would happen upon arrival in the new time zone) would cause a westward phase delay (opposite to what is needed for eastward travel). So, the eastward traveler should avoid bright light and/or wear sunglasses until after the habitual time of awakening in the home time zone; then the traveler should expose him/herself to bright light. Each day the time of exposure to bright light can be advanced by 1-2 hours.

When traveling west, the traveler should remain awake during the trip (using caffeine and naps strategically). Exposure to bright light should occur during the entire trip and until just before bedtime in the new time zone.

Treatment of jetlag

Short trips

One possibility is to keep to your usual schedule, in your home time zone

Or you can take sleeping pills for a few nights to put you on the new schedule

And/or you can use wake promoting agents, like modafinil and stimulants, to promote awakening in the new environment

Long Trips

Begin a few days prior to travel by timing bright light exposure progressively later in the day (for a westbound trip to delay cycle) or earlier in the morning (for an eastbound trip to advance cycle)

Light boxes can be used (containing light with wavelengths in the blue range)

Give melatonin in the early evening to phase advance the clock (going east) or in the morning to delay the clock (going west)

Doses of melatonin should be "circadian," not pharmacologic (e.g., 100 mcg every hour for 34 hours not 310 mg in a bolus dose for

Move towards the new time zone by 1-2 hours per day (whatever you can tolerate)

Use melatonin and dark glasses to manage light and circadian timing

Give a low dose of melatonin (300 - 500 mcg, or 0.5 mg) about 4 hours before desired bedtime

Give a bolus/large dose of melatonin (3-5 mg) an hour before bed if needed

School start times & their effects on kids

Damn Those Kentucky Drivers

Nearly 10,000 students in one Kentucky County, grades 6 - 12, provided self-report on sleep habits (bed and awake times), naps, daytime functioning, and difficulty staying awake in 1998 & 1999.

During Year I, schools started at the usual time (7:30 AM for high school & 8 AM for middle school)

During Year II, schools started one hour later (8:30 AM for high school & 9 AM for middle school)

Auto accidents dropped by 16.5% in Year II Teen auto-accidents increased by 8% in Year II

Land of 10,000 Lakes

Edina and Minneapolis changed their school start times from:

7:15 AM to 8:40 AM (Minneapolis) 7:25 AM to 8:30 AM (Edina) Students tend to keep the same bedtime when start time is delayed, so kids do, in fact, get more sleep (by 1 hour in this study) when school start time is delayed

Findings included: Less EDS, less sleepy during homework, less tardiness, & better attendance

Top 10% of students increased SAT scores from 1288/1600 to 1500/1600

Later start times = more sleep

Autonomic Nervous System in sleep (cardiovascular, gastrointestinal, respiratory)

Largely involuntary system

Preserves homeostasis

Regulates multiple organ systems

Highly integrated system

Centers located throughout CNS

Two branches

Sympathetic Nervous System (SNS)

Parasympathetic Nervous System (PNS)

Sympathetic (fight-flight or freeze)and parasympathetic (rest and digest)

Pulling an all-nighter, being exhausted at 2am but energy comes back at 10am

ANS is physiologically important during:

Transition from wake to sleep

Normal architecture changes associated with the sleep cycle (non-REM, SWS, REM)

Maintenance of

Blood pressure (CV events)

Gastric acid secretion (GERD)

Renal function

Breathing (OSA & asthma)

Endocrinology of sleep

Hormone release

Process C vs. S

Hormone release is influenced by:

Circadian Rhythm (Process C)

Sleep-Wake Homeostasis (Process S)

Environmental factors, such as postural changes, stress, food intake and exercise also modulate hormone release

You need to sleep to grow healthy

Growth hormone and Plasma Prolactin is under process S

Process S is sleep debt

ProcessC is circadian rhythm

Cortisol is under process C

Grehlin & leptin

Leptin is high throughout the night

Leptin → decrease in appetite

Ghrelin → increase in appetite

Immunology

Chronic sleep loss is associated with obesity, diabetes, CV disease, HTN

All are associated with inflammatory processes

Sleep deprivation in some lab animals leads to septicemia and death

Sleep is dramatically altered during infection

Human infection with influenza or rhinovirus leads to increase SWS

Bacteria, virus, yeast, and protozoan infections alter sleep

Sleep and thermoregulation/temperature effects

When we sleep our body temperature decreases

Sleep onset is associated with a dramatic reorganization of thermoregulatory control

Core Body Temperature (CBT) falls at sleep onset, accompanied by heat loss mechanisms (vasodilation & sweating)

Fall in CBT and slowed metabolism presumably contribute to an energy conservation function of sleep

Thermoregulation is less responsive during sleep (more responsive in NREM than REM)

In general sleep is best in humans at night when the CBT is low and melatonin is high

Sleep onset latency is minimized if sleep is initiated about 5 hours before minimum CBT

Electric blankets that increase CBT slightly cause increased nocturnal awakenings

Spicy meal increase in CBT by 0.2 C led to a decrease in SWS

There is some evidence that soporifics induce sleep in part by increasing peripheral body temp and decreasing core (BZDs & melatonin)

Caffeine has the opposite effect by increasing CBT

Sleep hygiene Definition and Typical sleep hygiene measures

A series of recommendations and practices designed to improve sleep quality, quantity, and daytime alertness, including the typical measures:

Environmental (e.g., temp, noise, light)

Scheduling (e.g., sleep/wake schedule)

Practices (e.g., bedtime routine)

Physiological (e.g., exercise, meal timing, caffeine)

Often advised by healthcare practitioners, although the evidence-base is not significant for most of the recommendations

Validity of sleep hygiene data

It's difficult to find any two studies with an identical set of recommendations

Most of the data supporting specific behaviors comes from studies of normal adult sleepers (not insomniacs)

American Academy of Sleep Medicine has found insufficient evidence to use sleep hygiene as a stand-alone treatment for insomnia (1999)

Research studies often use sleep hygiene as an "active placebo" making it difficult to determine its potential as a stand alone treatment

Almost all of our sleep hygiene data comes from studies of adults

The vast majority of the data appears relevant to older adolescents, college age, and emerging adults

You can extrapolate to children...or not

Caffeine Effects

Caffeine also causes increased neuron firing indirectly via the hypothalamus and pituitary gland

The hypothalamus senses that adenosine is blocked and (probably) thinks that some sort of emergency is happening (b/c the brain isn't relaxing as usual); it sends a message to the pituitary gland

The pituitary tells the adrenal glands to release adrenaline (epinephrine) and cortisol (a stress hormone), resulting in "fight or flight"

90% of americans consume caffeine in one form or another every day

More than half of americans consume more than 300 mg/day

The FDA and AMA consider 400 mg/day the upper limit of a moderate daily dose

20 - 30% of Americans consume more than 600 mg/day

Stimulates us, blocks adenosine receptors

FDA recommended limit of 400mg

If it sits in the water and brews longer then it will be stronger and have more caffeine

Caffeine Physiology

To a nerve cell, caffeine looks like adenosine

Caffeine competitively binds to the adenosine receptor, but unlike adenosine, caffeine doesn't slow down the brainl it just blocks the receptor

So instead of slowing down, the nerve cells keep going strong

Caffeine also causes the brain's blood vessels to constrict b/c they block adenosine's ability to open them up

Caffeine also inhibits acetylcholinesterase, so the duration of acetylcholine, another NT, is increased in nicotinic and muscarinic receptors in the CNS

How does caffeine contribute to wakefulness?

- Blocks. adenosine

- Fight or flight

- Brain isn't relaxed as usual

Alcohol (effects on sleep)

Alcohol/drugs → Alters sleep architecture, causes a block of stage 1 and rem

Alcohol increases NREM and reduces REM and Stage 1 in the first sleep cycles

Tobacco (effects on sleep)

Nicotine → Alters sleep architecture, decrease in restful sleep

Tobacco increases sleep latency and stage one sleep decreasing SWS, restful sleep and sleep time

Cigarette smokers have many sleep related complaints

PSG study of 6400 subjects found increased sleep latency (5.4 min), less total sleep time (14 min), more Stage 1 sleep, and less Slow Wave Sleep

No differences in sleep architecture between former and non-smokers

Analysis of sleep EEGs found less delta power (SWS) and higher alpha power

Nicotine is thought to exert its strongest effects on sleep architecture at the beginning of sleep but then exert effects of nicotine withdrawal later in sleep epoch

Nicotine

Dose dependent- - lower doses tend to stimulate REM and higher doses suppress REM

Rebound upon discontinuation increases wake time and decreases Stage 3

Withdrawal begins 6 - 12 hours after last use and can last 3 weeks

MJ (effects on sleep)

Delta-9-tetrahydrocannabinol (THC), the main active ingredient in MJ that gets you "high", has effects on sleep that has been known about since the '70s

THC is known to decrease both SWS and REM

Regular users generally report fewer dreams than occasional or non users

When regular users stop using MJ, they often report a REM rebound effect and a period of vivid dreaming

Implications?

THC decreases SWS and REM, less dreaming

Melatonin & ways to use it (sleep onset vs. chronotype adjustment)

Adjust the CBT set-point, allowing more blood flow to distal areas of the body and cooling of the core

sleep-promoting

Napping, Timing

When to Nap

Take advantage of circadian "windows of opportunity"- e.g., when clock dependent alerting is low and melatonin is high

2 AM - 5 AM (corresponds to lowest daily CBT)

2 PM - 5 PM (corresponds to midday melatonin surge)

But if you cannot, nap when you can

Great, adds up, encouraged,

No nap vs 5,10, 20 and 30 min naps, 24 young adults, good sleepers, not regular nappers held to 5 hours sleep for one night then given a nap opportunity at 3pm with 3-hours of post nap testing

Strategic napping

Preventative (before an activity that will make you tired - e.g., a long evening drive, shift work, physicians on night float, etc.)

Operational (on the job)

Short naps (20 - 30 minutes) avoid sleep inertia (e.g., the grogginess that you feel upon awakening from deep sleep)

Power naps (20 min Stage 2 nap)

Caffeine nap

Long naps (30 - 180 minutes) are more rejuvenating but also are more likely to interfere with the sleep cycle

Napping Benefits

Numerous studies confirm that daytime naps are sufficient to induce performance improvements in declarative and procedural memory

45 minute early afternoon nap, dominated by Stage 2 (slight SWS/REM), resulted in improvements in procedural (not declarative) memory (Backhaus & Junghanns, 2006)

Napping may benefit cardiovascular health

A 6 year study of greek men found that those who napped at least 3x/ week had a 37% reduction in CV related deaths (Naska et al, 2007)

Naps may reduce stress and BP (Zaregarizi, 2007)

These studies are possibly confounded

Bedtime snacks

A small snack before bed has been shown to promote sleep by keeping hunger at bay

The most sleep promoting foods are rich in tryptophan, a precursor of serotonin & melatonin, which induce sedation

Warm milk, turkey, and chamomile tea are all high in tryptophan

Good but not too close to bedtime

Exercise with sleep

Data are mixed

Little evidence that morning exercise affects sleep

Physical activity can increase sleep latency on the MSLT

Exercise later in the day may increase the depth of sleep, demonstrated by increase in SWS and total sleep time

But exercise just before bed may increase sleep latency

And research suggests that core body temp may be what matters, not exercise

Not within 4 hours of bedtime

Teaching infants/children to sleep through the night (techniques)

Extinctions

Positive Bedtime routines

Faded bedtime

Bedtime pass

Reinforcement

Sleep fairy

Alternative treatments

Extinction (unmodified, graduated, with parental presence)

Eliminate the associations

modifying environment of infant to help them put themselves to sleep

- establish regular sleep and wake time

- Create a relaxing bedtime ritual

Unmodified extinction

Child is placed in bed while any sleep interfering behaviors are ignored until morning

Ignoring is discontinued if child is ill, in danger, or becoming destructive

Graduated extinction

The extinction procedure is combined with checking procedure that is faded over time

Parents wait for progressively longer periods of time prior to responding to the child

Parents decrease the time they spend with the child over time

Extinction with parental presence

The parent is instructed to sleep in the same room with their child, but in a different bed, ignoring the child's crying or attempts to get out of bed

This sleep arrangement continues for 1 week, then the parent returns to sleeping in a separate room

This approach appears to reduce nighttime awakenings while limiting the post-extinction response burst

Positive Bedtime routines

Same every night

Last portion in sleeping environment

Short and sweet, heading in one direction

Consistent bedtime environment

Faded bedtime

The child's bedtime is temporarily delayed approximately 30 min later than the typical sleep onset time (or the time he usually falls asleep)

Remove child from bed and keep him awake for 30-60 min if he does not fall asleep quickly

Once child begins to fall asleep more quickly, the bedtime is systematically faded 30 min earlier over successive night until the bedtime goal is reached

Reminds you of?

Sleep restriction

Bedtime pass

Bedtime pass is a modified extinction for children who exhibit bedtime resistance, including calling our leaving the room after bedtime

Provide child a card or "free pass" exchangeable for one permitted trip out of their room.

After the child uses the pass parents are instructed to ignore additional requests or crying

Reinforcement

Caregivers first identify a specific target behavior

Achieving the target allows a child to get a reward

Sleep fairy

Combines the use of a social story with tangible rewards

Social story consists of reading the tale of the "Sleep Fairy" who leaves rewards under the child's pillow contingent upon appropriate compatible behaviors

Alternative treatments for helping a child sleep on their own

Massage helps to relax and reduce stress. There is some evidence that massage was more effective than rocking

Chiropractic manipulations are less studied.

Hypnosis and self-hypnosis

Definition of a dream

No universally accepted definition

Almost all definitions include 3 features:

A dream is "conscious"

A dream is accessible to recall

A dream occurs during sleep

"A train of thought & images passing through the mind in sleep" (Funk & Wagnall)

"A vivid, complex, hallucinatory experience generally accepted as real by the dreamer, and having mostly logical progression in time" (Dement)

Methods to improve dream recall

Whatever has citicoline is good to remember dreams, not weed

To improve dream recall:

Make an effort

Keep a dream log or recorder by the bed

Keep an object in the room to remind you to log

Give the dream a "tag" or title

Write down or record as much as you can first, analyze after

Use the present tense in recording your dream

(helps with recall; & reverting to past tense suggests discomfort)

Highlight the feelings, action, and symbols

Avoid saying you do not remember

Medications to Improve Dream Recall (& Lucidity?):

Vitamin B6 (250mg?); for recall

Galantamine (4-8mg); for recall

Choline(250-500 mg+?); for recall

Silene Capensis/ African Dream Root (brewed into a tea); for lucid dreaming

Mugwort (1 punch dried herb to 1 pint boiling water, 5-10 minutes); for dream recall

Calea Zacatechichi (tea or capsules); for bth

Dream recall

Why is it so difficult?

Areas of the brain involved in forming memories (like the frontal lobe) are quiet and chemicals important for encoding memories (like certain neurotransmitters) are reduced

Plus, maybe we don't "want" to remember our dreams

Not super trustworthy - state change, time delay, visual dreams hard to describe, self censorship

Could be improved thru using dream logs, highlighting feelings/actions

Dream meds - vitamin b6, galantamine, choline, silene capensis, mugwort, calea zacatechichi

Dream Recall Problems

What might dream reports be less than 100% trustworthy?

State change (reporting a sleep experience when awake)

Time delay (dream reports are obtained after the experience, which can lead to forgetting and interference)

Visual imagery may be difficult to verbally describe

Censorship (we may not report embarrassing, violent, sexual and aggressive material)

Lucid dreaming

Lucid Dreaming: a dream in which the dreamer is aware he/she is dreaming

Seems real, aware you are dreaming

This phenomena was the subject of many books in the 20th century, which contained not only personal accounts of lucid dreaming, but also tools for lucid dream work.

Despite the cultural fascination with lucid dreaming, the phenomena remained largely unstudied by scientists

Despite the seeming prevalence of this phenomena, scientists are still unsure what structure within the brain induces lucid dreaming

Lucid dreaming has a tendency to occur later at night, when most REM occurs

Unlike regular dreams, in which the dreamer is largely led by the dream, in lucid dreams, the dreamer is able to take control of the dream content

Many lucid dreamers report that the dream possesses qualities which seem to be enhanced beyond the usual dream experience

False Awakening: when the dreamer thinks he/she is awake but is, in fact, still dreaming

Physiologic effects during dream sleep

NREM vs. REM

Sexual content

Awakening is often disorienting - sleep inertia is a factor

Mental activity occurs during sleep

Dreams do occur in NREM but harder to recall, can be affected by sounds

Sleep talking / sleep terrors associated with NREM parasomnias

Many of the physiological events in REM replicate what the body would do with an identical experience in the real world

Evidence suggests that dreams can occur in NREM and do not simply reflect recall of earlier REM sleep dreams:

It is possible to influence dream content by sounds delivered in NREM (e.g., phone calls, discussions, etc.)

Some NREM parasomnias (sleep talking & sleep terrors) correspond to reported dream experiences

Full dreams are sometimes reported upon awakening from NREM only (before the first REM period or after NREM naps)

Reports obtained upon awakening from NREM (especially deep sleep) are hard to evaluate because of the disorientation associated with sleep inertia

It is now believed that mental activity occurs throughout sleep

Much of NREM "dreaming" is considered sleep mentation

Abstract thoughts, fragmentary images, and isolated feelings

Dreams Senses

Unless blind, all dreams are visual

2/3 of dreams contain sounds

8% of dreams contain touch

All other senses occur in only 4% of dreams

Pain is extremely rare in dreams

One's own death almost never occurs in dreams

Depression/negative emotion/amygdala and dreaming

Negative dream content is typical of depression

More frequent nightmares

Increased hostility

More mundane, trivial, masochistic, vivid and disturbing content

Depression also induces reduced dream recall frequency and reduced length of dream reports

Negative emotion in depression and amygdala is more activated and more rem as well as negative dreams

Negative emotion in REM

The amygdala (aka "threat hub") is highly activated in REM

The amygdala is an area of the brain that is engaged when unpleasant emotions like fear or aggression are felt

This may help to explain the preponderance of negative emotion in dreams

Note: People with MDD experience a greater amount of REM and sooner in the sleep cycle, which may increase the proportion of negative emotion in sleep and contribute to their depression

REM Sleep Decreases Amygdala Activity

Two groups of individuals (n = 34) are shown 150 emotionally charged photos, which they rate for emotional intensity

The group that slept showed lower amygdala reactivity in fMRI when shown the images at Time 2

Those who slept also showed an increase in "top down" control (interconnectivity) of the amygdala from the vmPFC

Those who slept also demonstrated lower emotional intensity ratings when viewing the images at Time 2

Those who didn't sleep also showed hyperactive striatal activity (e.g., nucleus accumbens) or a greater interest in rewards (also with less prefrontal control)

PTSD/prazosin

Prazosin

Higher than normal levels of Noradrenaline (NA) are found in the CSF of people with PTSD and correlates to greater symptoms of PTSD

These high levels of NA may block people with PTSD from entering and maintaining REM

Prazosin treats HTN by reducing NA in the brain

Prazosin is often helpful for reducing nightmares in PTSD

Reduction in nightmares can reduce PTSD

When traumatized, norepinephrine is increased, prazosin decreases this

Nightmares

Some suggest that nightmares and bad dreams are necessary rehearsals left over from evolution to help us prepare for threats that may come our way

Wild animals, fire, etc.

These "primitive" dreams still occur in children

In adults, the modern version of these events is losing your wallet or having an auto accident

Dementia dreams are often "primitive" (loss of cortical functions)

AIM model (Hobson)

Consciousness is determined by:

Activation- total and regional brain activity levels

Input- activation generated internally and externally

Modulation-ratio of aminergic to cholinergic neuromodulation

With cholinergic activity on in REM, the limbic system is activated without the prefrontal cortex turned on to work out logical associations

Dreams originate "bottom up" from activation of the sensory cortex by the brainstem PGO waves, which are "interpreted" by higher order brain structures

Dreaming is the brain's best attempt at interpreting activating signals in a coherent manner, and contents of individual dreams

AIM Theory

Activated brain areas in REM include Theory) awareness, eye movements, instincts, vestibular sensation (body in space), memory consolidation, and emotions

Areas involved in the production of motor movements and processing of sensory information are also activated

Areas involved in primary reception of sensory info are not active; nor are dorsolateral prefrontal cortex areas

Thus, the difference between dreaming and wakefulness is where the "activation" comes from

External when awake internal when in REM

Consciousness, helps us understand dream sleep, the difference between wake and sleep consciousness

PGO waves

Ponto-geniculo-occipital waves

Originate in the pons, lateral geniculate nucleus (thalamus), and occipital cortex

Start in the pons and spread to the lateral geniculate nucleus (which resides in the thalamus) and then end up in the primary visual cortex of the occipital lobe

These are prominent just before REM

Waves that start right before rem, start in the pons and go up, gatekeeper

Neurochemical activity

- Dreams have no function but do have coherence and meaning

- Dreams are based upon stored memory representation

-Dreaming is due to complex neurochemical mixture of acetylcholine and dopamine (and serotonin, norepinephrine, and histamine are absent)

Dreams are "top down"

Freud versus Jung

difference between dreams

Freud- symbolic, unconscious, they are real, have meaning, what is going on with us which is hidden, latent and manifest content, dream condenses in many forms

The dream is a symbolic representation of some other meaning

Free association is used to uncover hidden meaning

Repression

"What is the dream repressing? What is it covering up?"

Sex was the primaty dtive underlying dream content

Dreams are a representation of unconscious conflict that psychoanalysis can resolve

Jung- dreams are real, were explored by amplifying, tell the dream and get deeper and deeper into the dream

The dream itself is factual

Amplification is used to identify the facts within the frame

Creative approach to interpretation

"What is this dream telling me? What is it for?"

Saw many possible explainations

Dreams reveal key aspects of our defended selves that must be integrated to make us whole

Insomnia Definition

Typical symptoms

Insomnia is characterized by subjective complaints about dissatisfaction with sleep quality or duration, difficulty falling asleep at bedtime, waking up in the middle of the night or too early in the morning, or non-restorative sleep

Most common single symptom of insomnia are having multiple awakenings or unrefreshing sleep

Insomnia (DSM-5)

Difficulties initiating sleep (in children without caregiver intervention)

Difficulties maintaining sleep characterized by frequent awakening or problems returning to sleep (in children difficulties to return to sleep without caregiver intervention)

At least 3 nights per week, for at least 3 months

Coexisting mental disorders and medical conditions do not adequately explain the complaint of insomnia

Typical Symptoms

-EDS, fatigue, low energy, bad move, cognitive impairment- difficulty functioning- Difficulties initiating sleep

flip flop switch

Insomnia Comorbidities

Adults with insomnia

> 5x comorbid anxiety or depression

>2x comorbid congestive heart failure

Compared those without insomnia (US National Health Interview Survey, 2002)

>3x comorbid anxiety, mood, impulse-control or substance use

(US National Comorbidity Survey, 2006)

Strong correlation between chronic pain and insomnia

Tang et al (2007) found that 53% of chronic pain patients suffered insomnia

Insomnia accompanies medical disorders in approx. 35% of cases

Insomnia is also causally associated with

Hypertension (high blood pressure)

Sensitivity to pain

Altered metabolic function

Insulin resistance, a condition associated with diabetes mellitus

Obesity

Cardiovascular morbidity

Higher level of physiological arousal

Elevated heart rate

Insomnia

Predisposing factors

before insomnia

personality/genetic

Sleep-wake cycle

Circadian rhythm

Coping mechanisms

Age

gender

Insomnia

Precipitating factors

life rating

illness

a loss

Situational

Environmental

Medical

Psychiatric

Medications

Insomnia

Perpetuating factors

maintaining factors, adressed in the CBT-I

Conditioning (negative)

Substance abuse

Performance anxiety

Poor sleep hygiene

excessive napping

half life

the process in which our body eliminates any medicine or drug

how long does it take until your body contains half of the dose in your body

Treatment of insomnia

Use of medication (no names required)

How medications work

Benzodiazepine receptor agonists (= increase GABA activity)

"non-benzodiazepine sleeping pills" or "Z drugs":

They bind to GABA receptor in the same area benzodiazepines act even if they are structurally different

Controlled substance but with less potential for abuse

They do not suppress SWS as much as Benzodiazepine

Sleeping pills induce a little more sleep, decrease sleep latency, people feel more rested because the medicines makes it difficult for memory to be encoded, so people forget they ever awoke in the night even though they did

Typical medication side effects

Potential adverse effects:

Residual effects

Confusion

Dry mouth

Constipation

Blurred vision

Difficulties urinating

- abuse

- lethal in overdose if in combination with other medication

- respiratory depressant

- suppress SWS

- sleep paralysis

- hallucinations

- decrease sleep latency

- anterograde amnesia

Treatment of insomnia

CBT-I

Cognitive Behavioral Therapy for Insomnia CBT-I:

Education about sleep

Sleep Hygiene

Sleep Cycles

Sleep Duration

Stimulus Control

Sleep Restriction

Cognitive Therapy

Relaxation techniques

Biofeedback

Visualization

Start with their sleep goals

E.g., reducing the amount of time awake in bed (as opposed to the number of hours asleep)

Validate that the behavioral changes they're about to start aren't easy and will be difficult

E.g., they must be very resilient to have come this far in life sleeping this poorly

Roll with resistance (e.g., people don't understand how much you're suffering)

Provide sleep education and start sleep logs

Photograph the sleep environment. Identify pros and cons

CBT-I stimulus control therapy

Assumes that there is a learned association between wakefulness and the bedroom

To break the cycle, the patient must not spend time wide awake in the bedroom

Go to bed only when sleepy

Do not use the bedroom for sleep-incompatible activities

Leave the bedroom if awake for more than 20 minutes

Return to bed only when sleepy

Do not nap during the day

Arise at the same time every morning

Not only use the bed only for sleep but also sleep only in bed in order to associate the bed only with sleep

Relaxing bedtime routine

No clock watching overnight

CBT-I sleep restriction

The basis of sleep restriction therapy is that, regardless of initial reasons for insomnia, one of the perpetuating factors for insomnia is staying in bed for a much longer time than one sleeps each night.

Sleep restriction serves to

Re-educate the body to sleep in a consolidated fashion

Increase propensity to sleep by increasing homeostatic sleep drive with partial sleep deprivation

Systematic reduction of time in bed to the amount of total sleep time from sleep log data

Behavioral treatments for pediatric insomnia

- consistent bed time

- sleep associations

- self-soothing skills

- bedtime fading

Unmodified extinction - ignored until morning

Graduated extinction - checking procedure faded over time

Extinction with parental presence - parent sleeps in same room, but different bed

Scheduled awakenings - parent awakens child prior to expected awakening times and gradually delayed

Delayed Sleep Phase Syndrome

Definition

Sleep disruption due to a misalignment between the endogenous circadian rhythm and the sleep-wake schedule required

The sleep disruption leads to excessive sleepiness or insomnia, or both

Delayed sleep phase type: A pattern of delayed sleep onset and awakening times, with an inability to fall asleep and awaken at a desired or conventionally acceptable earlier time

advanced sleep phase syndrome

wake up early go to bed early

a 4-hour advance in rhythms of sleep and temperature cycles, apparently caused by a mutation of a gene (per2) involved in the rhythmicity of neurons of the SCN

Delayed Sleep Phase Syndrome

Causes, prevalence and risk factors

Often corresponds with natural wake up times

Conforming to external social requirements can lead to sleep restriction

High energy, and alertness in evening

Difficulties falling asleep earlier, fogginess / low mood

Unsupervised time for adolescents (video games / TV)

Different effect of light on circadian rhythms depending on core body temperature

Body temp fluctuations / effect of light changes are in sync

Melatonin secretion is regulated by circadian rhythm, and light during night suppresses melatonin

Circadian rhythms misalignment

Difficulties falling asleep when expected

Forbidden zone (evening peak of alertness)

No daytime symptoms when allowed to sleep according to preference

Worsened by incorrect use of light and/or use of evening electronics

Majority of adolescents suffer from delayed sleep phase rather than insomnia

treatments for delayed sleep phase syndrome

Light therapy

Melatonin

Sleep phase chronotherapy

Circadian rhythm disruption treatment - melatonin timings before expected sleep time

2-4 hours before desired bedtime of melatonin dose

Light therapy

Light exposure in AM after lowest point of CBT

Light after latest wakeup time

30 minutes of light maintenance dose at wakeup time

Sleep phase chronotherapy

Moving bedtime - rising time later each day, stopping when sleep is on normal schedule

Definition of parasomnia

disruption of sleep

loss of REM atonia, act out dreams while dreaming

Undesirable physical or cognitive experiences occurring during specific sleep stages or during the transitions between awake and asleep states

Undesirable physical / cognitive experiences that occur during sleep stages or during sleep wake transition

Abnormal behaviors during sleep such as sleep terrors, nightmares, sleepwalking, and enuresis.

Nightmares occur during REM sleep.

Sleep terrors occur during stages 3&4 (delta sleep).

Sleepwalking is associated with stage 3 or 4 delta sleep in the first third of the night and with REM later in the night.

Childhood enuresis typically takes place within 3 to 4 hours of bedtime but is not limited to particular stages of sleep.

NREM parasomnias (or Disorders of Arousal DOA)

Disorders of arousal during NREM sleep

Sleep Terrors

Sleepwalking or Somnambulism(not actually dreaming)

Confusional Arousals

Sleep Related Eating Disorder

Sexsomnia

Behavioral and medication treatments for NREM parasomnia

Psychosocial Interventions

Repeat of a violent episode is rare

Family/patient education

Treat any primary disorders (SDB, RLS)

Avoid possible precipitants

Avoid sleep disruptions

Loud noises, limit evening oral fluid intake

Safeguard the home

Movement sensors, locks on windows, remove potentially lethal objects, etc.

Enforce afternoon naps (with Sleep Terrors)

Plan for scheduled awakenings

Medication

Risk factors NREM parasomnias (or Disorders of Arousal DOA)

Inadequate sleep

Irregular sleep schedule Fever, illness Sleeping with a full bladder

Sleeping in a new/unfamiliar environment Sleeping in a noisy environment (e.g., TV on) Stress, anxiety Medications (e.g., chloral hydrate, LiCO3, clonidine, TCAs)

Primary sleep disorders (e.g., OSA, PLMD, RLS) S

leep disruption (e.g., asthma, GERD, ear infection, pain, caffeine, EtOH, congestion)

Enuresis (bedwetting) and its treatments

- caused by primary enuresis

- occurs in kids

- nocturnal enuresis is associated with poor self image, diminished achievement in school, significant time by families compensating for the symptoms

Enuresis treatment

education

discontinue all caffeine

restrict late-night fluid intake

- afternoon nap

- brief wakening for the bathroom at midnight

- pelvic and bladder training

Nighttime fears

Animals, fictitious characters (e.g., witches & monsters), being kidnapped, or burglars

Anxiety is believed to predispose children to parasomnias and nightmares

Occasional nightmares occur in 80% of children

15% report frequent nightmares (>1/month)

69% of children report that the content of their nightmares is influenced by frightening material viewed on TV or at the movies

Positive self talk and coping thoughts

Desensitization and reinforcement

Relaxation

Deep breathing

Progressive muscle relaxation

Obstructive Sleep Apnea Definition

Obstructive events refer to moments in which there is cessation of airflow due to obstruction in the upper airway.

During these episodes, the muscles that promote breathing (the diaphragm and chest wall musculature) continue to work.

The obstruction is caused by the throat muscles relaxing, eventually closing the throat for short periods

Apneas can lead to moments of asphyxia (O2 decreases and CO2 increases)

During apneas, we awaken to restart breathing

Episodes can happen multiple times per hour through the sleep period

People are generally unaware of these occurrences

2 - 8% of the population suffer from OSA

Anatomy of the throat and pharynx (OSA)

Risk factors of OSA

Obesity (BMI >30), neck circumference >17" male, 16" female

Airway conformation

Gender: M>F

Menopause • Older age

Nasal problems (deviated septum, nasal polyps)

Family history of OSA/snoring

Consumption of alcohol or sedatives prior to bedtime

Exposure to cigarette smoking

Craniofacial abnormalities

Sleeping supine

Comorbid conditions (e.g., neuromuscular disorders)

Symptoms of OSA

EDS (Excessive Daytime Sleepiness)

Fatigue (not necessarily sleepiness)

Unrefreshing sleep ("I wake up more tired than when I went to bed")

Insomnia

Morning headaches (brain starving for O2)

Dry mouth (because they try to open their mouth to improve breathing)

Awaken to urinate multiple times per night

Bed partner complaints about snoring, apneas, choking sounds and restlessness during sleep

OSA SYMPTOMS IN CHILDREN

Sleep apnea occurs in about 2% of children; symptoms include:

Longer total sleep time than normal More effort when breathing (flaring nostrils, heaving chests, sweating); the chest may have an inward motion during sleep

Behavioral difficulties (e.g., hyperactivity and inattention)-ADHD-like ?

Irritability

Bed-wetting

Morning headaches

Failure to achieve expected growth and weight gain

Health consequences of OSA

Cor Pulmonale (& subsequent CHF and MI)

Hypertension

Stroke

Headaches

Obesity

Seizures

Diabetes

Pulmonary hypertension

Worsening of asthma

Snoring vs. apnea

SNORING

Habitual snoring is reported in 24 % of women and 40% of men and increases with age

Snoring may be a sign or a precursor of OSA

Old studies showed that habitual snoring might increase the risk for cardiovascular disease, stroke, hypertension, and EDS

However, many of these studies did not differentiate between simple snoring (primary) and snoring associated with obstructive sleep apnea

Apnea

Temporarily cessation of breathing

Apneas can lead to moments of asphyxia (O2 decreases and CO2 increases)

During apneas, we awaken to restart breathing

Sleep Apnea is defined as a recurrent, temporary cessation of breathing during sleep due to:

Obstruction

Tongue and/or tonsils & adenoids

Central

The brain fails to transmit signals to the breathing muscles

Mallampati Classification

anatomical inspection of upper airway patency, used to classify degree of intubation difficulty on a scale of 1-4

*the larger the number, the MORE obstructed

**1-2 = normal airway

**3-4 = problematic airway (difficult to intubate)

Treatment of OSA

Lifestyle changes -losing weight and avoiding alcohol and smoking (SAME for snoring)

If lifestyle changes do not eliminate OSA:

Positional therapy

Oral appliances

Traditional surgery / uvulopalatopharyngoplasty (UPPP).

Alternative surgery procedures (laser and radiofrequency tissue ablation, somnoplasty)

Continuous positive airway pressure (CPAP)

TRACHEOSTOMY

The original treatment

The surgeon makes an opening through the neck into the airway & inserts a tube

Nearly 100% successful

Requires a quarter-size opening in the throat, producing potentially other medical and psychological problems associated with recovery.

Today, this operation is performed rarely, usually only if sleep apnea is life-threatening.

Narcolepsy & cataplexy Definition

The two primary symptoms in narcolepsy are related to its name (numbness attack):

Excessive daytime sleepiness, with frequent daily sleep attacks or a need to take several naps during the day

The naps or "attacks" are refreshing

Temporary and sudden muscle weakness (cataplexy), usually brought on by strong emotions, such as laugher or, less frequently, anger

The muscles most frequently involved are knees and jaw

Cataplexy is a unique and distinctive symptom for narcolepsy (pathognomonic)

Narcoleptics experience all stages of sleep but start by going directly in REM

Narcolepsy & cataplexy Symptoms

Micro-sleep episodes, in which the patient behaves automatically but without conscious awareness (automatic behaviors)

Sleep paralysis

REM Intrusions

Dreamlike states between waking and sleeping (called hypnagogic hallucinations )

Sleep Onset Rapid Eye Movements Periods (SOREMP)

Proposed etiology (Narcolepsy & cataplexy)

Autoimmune response

Hypocretin/orexin

Narcolepsy is a neurological sleep disorder

It is not caused by mental illness or psychological problems

It is most likely the end result of a number of genetic abnormalities that affect specific biologic factors in the brain, coupled with an environmental trigger such as a virus.

People who develop narcolepsy have a predisposition to developing an autoimmune disorder which leads to the destruction of hypocretin (orexin) cells

Some data suggests that the flu vaccination and flu infection are related to narcolepsy

Hypocretin (orexin) level in the CNS

People who develop narcolepsy have a predisposition to developing an autoimmune disorder which leads to the destruction of hypocretin (orexin) cells

damage to hypothalamus

Von Economo's Inferences

(dotted lines)

*Diagonal hatching = hypersomnolence

*Horizontal hatching = insomnia

*Lesions at the arrow induce narcolepsy

These findings suggested to Von Economo that these two areas were the neural circuitry of sleep and wakefulness

Von Economo learned that there are two ares responsible for the neural circuitry of sleep and wakefulness. Lesion to one area lead to hypersomnolence and lesion to another area lead to insomnia. A lesion in between these sites leads to narcolepsy.- HLA (immune system maker), found in 100% of people with narcolepsy

Treatment (Narcolepsy & cataplexy)

Education

Patients, family, friends, & employers

Sleep hygiene

Safety regarding driving and occupational hazards

Doctors are under no obligation to report in NY state

Patients "must" be symptom free for one year if known to DMV and are driving (doctor attestation)

Strategic napping: Two 15 minutes naps per day usually after lunch and around 5 pm

Medications

Cataplexy

Gamma-Hydroxybutyric acid (GHB)

Xyrem

Antidepressants with an action on

Noradrenalin (norepinephrine) and serotonin

Venlafaxine

Atomoxetine

Clomipramine

Sleep Attacks

Gamma-Hydroxybutyric acid (GHB) Xyrem

Modafinil & Armodafinil

Concerta (methyphenidate)

Other stimulants

Restless Legs Syndrome (RLS) Symptoms

a neurological disorder characterized by uncomfortable feelings in the legs, producing a strong urge to move themAn urge to move legsHappens when you're sitting or lying downRelieved by movement (walking)Worse in evening or night

Nocturnal cramps:

Painful and palpable muscular contractions.

Relieved with stretching.

Painful peripheral neuropathy:

Sensory symptoms described as numbness, burning, and pain.

Typically not relieved while walking or during sustained movement.

Arthritis:

Discomfort is centered in the joints.

Volitional movements:

Occurs in fidgety patients, during times of anxiety or boredom.

Typically lack sensory symptoms, discomfort, or the urge to move.

Positional discomfort:

Associated with prolonged sitting or lying in the same position, relieved by changing position.

Periodic Limb Movement Disorder (PLMD) Symptoms

legs jerk 2-3 times per minute during sleep, differs from RLS which occurs during wakeful rest periods as well

Brief limb jerks during sleep (esp legs)

Begin near sleep onset and decrease in stage 3 and REM Movements are rhythmic, every 20-60 seconds, causing repeated and brief arousals People are usually unaware but c/o insomnia and EDS Although most people with RLS experience PLMS, the opposite is not true PLMS diagnosed by polysomnography, while RLS is a subjective diagnosis Association with ADHD, RLS, SDB, Tourette's and iron deficiency

URGE criteria

URGE diagnostic criteria: URGE

Urge to move limbs

Rest or inactivity precipitates or worsens symptoms

Getting up or moving improves the sensation

Evening or nighttime apparence or worsening symptoms

Supportive features: sleep disturbances, PLMS (80% of the cases), positive FH, positive response to tx

Diagnostic Criteria for RLS

1. An urge to move the legs usually but not always accompanied by or felt to be caused by uncomfortable and unpleasant sensations in the legs.

2. The urge to move the legs and any accompanying unpleasant sensations begin or worsen during periods of rest or inactivity such as lying down or sitting.

3. The urge to move the legs and any accompanying unpleasant sensations are partially or totally relieved by movement, such as walking or stretching, at least as long as the activity continues.

4. The urge to move the legs and any accompanying unpleasant sensations during rest or inactivity only occur or are worse in the evening or night.

5. The occurrence of the above features are not solely accounted for as symptoms primary to another medical or a behavioral condition (e.g., myalgia, venous stasis, leg edema, arthritis, leg cramps, positional discomfort, habitual foot tapping.)