Disorders of Sleep
Insomnia
Narcolepsy
Sleep Walking
My day out with narcolepsy
• Watch the clip.
• What is life like from this mans
perspective.
• How does his sleep disorder affect
his life?
Disorders of Sleep - Insomnia
Insomnia
Narcolepsy
Sleep Walking
My day out with narcolepsy
• Watch the clip.
• What is life like from this mans
perspective.
• How does his sleep disorder affect
his life?
Disorders of Sleep - Insomnia
A
C
E
Evaluate the risk factors for Insomnia
Give some explanations for primary
insomnia
Describe the difference between primary
and secondary insomnia
Check it out…..
• http://www.bbc.co.uk/science/humanbody/sl
eep/
Two categories of sleep disorder
Type
Description
Daytime
sleepiness?
Examples
Dysomnias
Problems with
amount or
quality of
sleep.
Yes
Insomnia
Narcolepsy
Parasomnias
Behavioural or
physiological
events during
sleep
Not usually
Sleep walking
Night terrors
Insomnia
• What is it?
• More than just “ I can’t sleep”, we all get that
from time to time, maybe because we are
stressed, anxious or excited.
• To be diagnosed with insomnia you need
proper diagnostic criteria.
Diagnosing Insomnia- criteria
Takes more than 30 min to fall asleep
Spend less than 85 % of time in bed actually
asleep
Wake up frequently
Suffer at least 3 times a week
• Must last longer than a month to be
diagnosed as clinical insomnia!
Primary and secondary insomnia
• Quite often insomnia can be caused by
another medical or psychological condition,
e.g. depression. In these cases it is known as
‘secondary insomnia’
• Primary insomnia is chronic insomnia where
there is no other medical condition that might
explain it.
This is important for treatment!
Primary Insomnia
• There are a few different types of primary
insomnia
1. Psychophysiological insomnia
2. Idiopathic insomnia
3. Sleep state misperception
1) Psychophysiological insomnia
• Learned or Behavioural Insomnia
• A vicious cycle of worry and stress!
1) Psychophysiological insomnia
• Fall asleep in front of the TV
but not in Bed?
• It is suggested that this
occurs because the learned
associations are not present
in the new or unfamiliar
sleep environment.
Primary Insomnia
• Treatment for learned
insomnia aims to improve
sleep habits and reduce
unnecessary worry.
1) Research on psychophysiological
insomnia:Dauvilliers et al (2005)
• Dauvilliers asked 256 consecutive primary insomniacs to
complete a clinical interview, psychometric questionnaires, a
questionnaire on the family history of insomnia and, when
indicated, a polysomnography (a series of detailed
physiological recordings of their sleep).
• A control group was also used to obtained an estimated
base-rate incidence of insomnia in their families. Results
showed that of those patients with primary insomnia (n=77),
72.7% reported familial insomnia compared with 24.1% in
the non-insomnia control group.
• These findings suggest a familial link to primary insomnia.
Primary Insomnia
2) Idiopathic Insomnia
• This was originally called childhoodonset insomnia because it tends to
occur at a very early age.
• It is thought to occur due to an
abnormality in the brain mechanisms
that control the sleep-wake cycle.
• It is suggested that a neurochemical
lesion exists in the sleep system, in
which patients tend to be on the
extreme end of the spectrum towards
arousal and thus have an inability to
sleep normally.
Primary Insomnia
3) Sleep state misperception
• When asked about sleep, these people underestimate
their total sleep time and overestimate the time it
took them to fall asleep.
• Dement (1999) cites a case where a patient who
complained of severe insomnia was asked to sleep for
10 consecutive nights in the sleep lab. Each morning
he was asked to complete a questionnaire where he
had to estimate how long he took to fall asleep each
night. He reported times ranging from 1 to 4 hours to
fall asleep, with a mean of 90mins. According to
Dement’s sleep lab recordings, he never took more
than 30mins to fall asleep and the mean was 15 mins!
Primary Insomnia
Secondary Insomnia (More common)
• There are a number of physical and psychiatric causes of
secondary insomnia, including the following:
– Hormonal changes in women, these include premenstrual syndrome,
menstruation, pregnancy and menopause.
– Decreased melatonin production: the levels of melatonin, the
hormone that helps control sleep, decrease as a person ages. By age
60, the body produces very little melatonin.
– Medical conditions: many medical illnesses can disrupt sleep and
produce insomnia. These include allergies, arthritis, asthma, heart
disease, high blood pressure and Parkinson’s disease.
– Psychiatric conditions: secondary insomnia is a common symptom of
depression. It is also associated with anxiety disorders, PTSD and
dementia.
Explanation 1- it’s Psychological
• Insomnia is a learned response to night time cues,
you need to unlearn your current cues and get some
new cues- a new bed time routine!
• The fact that this works is evidence that this is the
problem!
–
–
–
–
Only go to bed when sleepy
Only use your bedroom to sleep in, not work or watch TV
Get up at the same time every day
Do not take naps
Explanation 2- its down to high levels
of arousal
• High levels of arousal, whether it is down to
anxiety, depression or anxiety about sleep
itself are likely to interfere with the brains
sleep mechanisms.
• How do we solve it? CBT or relaxation
techniques
Explanation 2- Solution: CBT
• “ I won’t sleep” “I need sleep” “if I don’t sleep, I
won’t cope tomorrow!” The more someone with
insomnia tries to sleep, the more anxious they get!
• CBT challenges some of these assumptions and
reduces anxiety.
• Again, the fact that it works is evidence for this
explanation (ditto relaxation techniques).
Explanations for Insomnia
• Whilst you don’t strictly speaking need to
know about treatments for insomnia- if a
treatment works well, it is likely to be
because it has something to do with the
cause of it, so it isn’t a waste of time!
1. It’s psychological
2. Its down to high levels of arousal
3. Its faulty brain mechanisms
Explanation 3- Faulty brain
mechanisms
• The most prescribed psychological drug over
the last 40 years has been nitrazepam (aka
Mogadon), which was a sleeping pill.
• Whilst it does increase the time spent asleep,
it interferes with the normal ultradian
patterns. They lead to morning sleepiness and
make the insomnia worse when you stop
taking them!
Explanation 3 contd
• Obviously, if the insomnia is secondary to
another complaint- then drugs to treat the
original problem will also reduce the insomnia
Personality Factors and Genetics
• How much sleep do you need a night?
Einstein needed 10 hours, Margaret Thatcher
only needed 4!
• It seems to vary, the average people GET is
about 7.5 hours a night, 16% get less than 6.5,
16% more than 8.5 hours. (not much variation
there!)
Personality
• So what is it that means some people need
more, or less?
• Neuroticism seems to be associated with
insomnia (Heath et al 1998, did a twin study
that showed higher neuroticism  more
insomnia).
Personality- Chronotype
• Are you a ‘morning person’ or an ‘evening
person’? A ‘lark’ or an ‘owl’?
Larks and Owls (chronotypes)
• The circadian rhythms of larks is roughly 2 hours
ahead of owls and this difference is genetic.
• Chronotypes are stable over seasons and lifetimes,
controlled by endogenous pacemakers, controlled by
‘clock’ genes.
• A distinct personality trait that is genetically
determined!
Chronotypes- so what
• Well, not much- but maybe owls should not
try to go to bed too early! And Larks just
shouldn’t try to stay up too late!
Plenary
•
•
•
•
You are suffering from a sleep disorder – describe your
symptoms (write them down) 2mins
Pass your symptoms along 4 people
Now diagnose the patient who has been passed to you– how
will you treat this client? Why?
Investigating Insomnia worksheet
Essay Questions Outline and evaluate explanations of two or more sleep disorders (24 Marks)
PPP Factors
Predisposing
Genetics
Precipitating
Environmental Stressors
Perpetuating
Stress due to sleep problems!
Narcolepsy
• Describe the symptoms of Narcolepsy
• Outline and evaluate explanations for
Narcolepsy.
REM hypothesis
Mutation in HLA
Hypocretin
Narcolepsy
First identified as a medical condition in early
20th century.
Onset is early adulthood or adolescence but can
occur early or later in life
Affects about 0.5-1 in 1000 people worldwide so
very rare.
http://www.youtube.com/watch?v=3MBCeK
n0Oeo
Narcolepsy Symptoms
4 general symptoms associated with Narcolepsy:
1) Excessive daytime sleepiness and sudden sleep attacks:
These can occur at anytime (even while eating or driving).
An episode lasts about 10-20 mins.
2) Sleep paralysis: A consciously experienced inability to
move just prior to falling asleep or waking up.
3) Dreamlike experiences: whilst still awake and just before
falling asleep or just before being fully awake
4) Cataplexy: Skeletal muscles weaken or are paralysed and
the person collapses and enters REM sleep. It is often
triggered by an emotional event (Laughter or anger)
Explanations for Narcolepsy
The REM hypothesis
The narcolepsy-HLA link
Hypocretin
Explanations for Narcolepsy
The REM hypothesis-A kind of REM sleep at an
inappropriate time (Popular explanation in 1950s)
Malfunction in the system that regulates REM
sleep
In cataplexy neurons in the medulla, which are
active during REM and suppress skeletal muscles
are activated when they shouldn’t be.
It explains some of the symptoms of narcolepsy,
such as lack of muscle tone (Cataplexy) which
match REM sleep
Explanations for Narcolepsy
Evidence for The REM hypothesis
Vogel (1960) observed sleep patterns during
narcoleptic episodes in one patient and found
(as predicted) that REM patterns were present at
the beginning of each episode.
Siegel (1999) recorded activity in brainstem of
narcoleptic dogs and found the same activity
during cataplexy as found in REM sleep.
However… generally research support has not been
convincing.
Explanations for Narcolepsy
Mutation in HLA
Possibly linked to a mutation of the immune
system.
Honda et al (1983) found increased frequency of
one type of human leukocyte antigen in
narcoleptics.
However..unlikely to be the sole explanation as HLA
mutation was found in some but not ALL
narcoleptics and also common in the general
population (Mignot et al 1997)
Explanations for Narcolepsy
Hypocretin (neurotransmitter)
1990s American research team found that mice who
could not make the neurotransmitter called hypocretin
(aka orexin) displayed sleep attacks and cataplexy
Lin et al (1999) found some strains of dogs (Labradors &
Dobermans) also exhibited narcolepsy following
excitement. The researchers identified a mutant gene
on chromosome 12 in the dogs which affects neurons
that secrete hypocretin.
Narcolepsy
Hypocretin-secreting neurons are normally active during
wakefulness and keep the brain from shutting down
unexpectedly. So, narcolepsy is caused by a deficiency of
hypocretin.
Supported by stimulant drugs used to treat narcolepsy in humans
and dogs work by activating hypocretin- containing neurons.
hypocretin levels in the cerebrospinal fluid of narcoleptics are v
low and narcoleptics have lost 90% of hypocretin-secreting
neurons from the hypothalamus (Nishino 2000)
Low levels of hypocretin are not linked to inherited factors
because narcolepsy doesn’t run in families (Mignot)
Sleep walking
• Describe the symptoms of Sleep Walking
• Outline and evaluate explanations for Sleep
Walking
Sleep walking (Somnambulism)
Is an example of a parasomnia
Most common in childhood,(age 4-6) affecting
20% of children and less than 3% adults (Hublin
et al 1997). More common in boys
Occurs during NREM/SWS related to night terrors
Walk around as if awake, involves ordinary behaviours like
dressing or making food.
A sleep walker is not conscious and later has no memory of
events during sleep walking
Sleep Walking
• Sleepwalkers are difficult to wake
• Each episdode can last for a few seconds or
minutes
• It is not dangerous to wake a sleep walker up
Explanations
Incomplete arousal
EEG recordings of sleepwalkers show delta
waves (typical of SWS) and beta waves (awake
state)
Seems that it occurs when a person in SWS is
awakened but arousal of brain is incomplete.
This abnormal arousal is likely to be genetic
Explanations
Other factors
Increase likelihood of SW such as sleep
deprivation
Alcohol
Fever
Stress
Hormonal changes in puberty
A.I.Ds Nature & Nurture
Can be explained by the Diathesis-Stress model
Genetic basis for SW
Prevalence of SW in first degree relatives is 10X greater than the
general population (Broughton 1968)
50% concordance in MZ twins compared with only 15% in DZ
twins
Gene identified for sleep walking (DQB1*05 gene)
Environmental component
Maturity of brain circuits-immaturity leads to SW
Amount of SWS e.g. factors such as sleep deprivation increase
SWS so SW becomes more likely
Being a child is related to all of above (immature and high levels
A.I.Ds Real World Application
Research has suggested a way to diagnose
vulnerability to sleep walking.
40 patients referred to a clinic for suspected SW
were observed before and after 25 hours of
sleep deprivation. Before sleep deprivation
50% of the patients showed episodes of SW
and after it rose to 90%.
A.I.Ds Real World application
Cases of murder
Is a person really sleepwalking?
E.g. Jules Lowe killed his father & Brian Thomas
killed his wife
Plenary
•
•
•
You are suffering from a sleep disorder – describe your
symptoms (write them down) 2mins
Pass your symptoms along 4 people
Now diagnose the patient who has been passed to you– how
will you treat this client? Why?
Essay Questions Outline and evaluate explanations of two or more sleep disorders (24 Marks)
Sleep specialist
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Review case histories of patients, make diagnoses, and recommend treatments.
You have the primary information for the two case histories .
Write down what you consider to be the key aspects of their patients’ sleep disorders in
the appropriate box on the Sleep Specialist’s Evaluation Form
Using Sleep Disorders Reference Manual. Make a preliminary diagnosis for each case
history. Write your preliminary diagnoses in the appropriate boxes on their evaluation
form.
List the matching symptoms of the sleep disorders that match the key aspects of your case
histories.
Some additional information regarding each case has come to light you will be given some
Secondary Information.
Read the Secondary Information for each case and use this new information to re-evaluate
your diagnoses.
If students have changed a diagnosis, you should enter the new diagnosis, together with
the reason for the change, in the appropriate boxes on the evaluation form.
Recommend a treatment.
You will be given the bottom portion of the appropriate case histories that contains
discussion questions to complete