Lecture 4 Flashcards

1
Q

What are the different ways to investigate human sleep and advantage and disadvantages

A
actigraphy 
sleep diaries 
MSLT
MWT
PVT
sleep questionnaires
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2
Q

sleep recordings and sleep patterns and behaviours help us investigate sleep

A

SLEEP RECORDINGS

brain acitivty
Muslce Activity
MSLT
Sleep Architecture

SLEEP PATTERNS AND BEHAVIOURS
Sleep diareis
acitigraphy
questionnairres (ESS, SSS, PSQI, ISS, Berlin, MCG)

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3
Q

What is fragmentation index what is it measure by what is patholgical?

A

total number of awakenings or shifts to n1/total sleep time in hours)
<85% suggests poor sleep efficiency

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4
Q

brain actiivty

PSG (6) T Se so wasp a fi
PET

Muscle activity

A

PSG -
allows investigation of TST, Sleep efficiency, sleep latency, wake after sleep offset, number of awakenings, fragmentation index (total number of awakenings or shifts to N1 / total sleep time in hours)
<85% suggests poor sleep efficiency

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5
Q

Sleep diaries

A

more global iew of patterns and behaviours

enhanced information but without the accuracy of PSG or actigraphy

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6
Q

actigraphy

A

more complex than sleep diaries

validated against PSG useful for estimating total sleep time, sleep % and WASO

can’t say that sleep period of no mvoemnt as there’s some movement but generally movement correlates well with sleep

cheap and tolerated well by peaditirc clincial popualtion
Insight to CR dioder used on normal sleep enviornment for long periods

may be inaccurate in elderly

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7
Q

Sleep questionaiires

A

Epworth = day time sleepiness (when doing a certain acitivty how sleepy are you)

Berlin = breathing realted how often do you snore etc

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8
Q

MWT and how does it diagnose sleep disorders

Test session terminated when unequivocal sleep occurs or after XX mins
tests are repeated after X hours

there are X-X trials in total

Ability to remain awake for XX mins is the strongest evidence for normal alertness
sleep onset less than X mins (longer than MSLT) considered abnormal

A

measures maifest sleepiness based on the idea that aiblity to stay awake may be more important to know than ability to fall asleep

subjects instructed to stay awake
Test is performed in a dimly lite room on a bed with no addition acitivites

patients have PSG at the same time so thier sleep can be assessed

40 mins 
2 hours 
4-5 trials in total 
40 
8

between trials only restriction is can’t go out into daylight

can be used to evlaute riskif someone’s jon involves public transport/saftey - some occupations require a MWT to be conducted

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9
Q

How might you investigate day time sleepiness?

A

physiological- biological drive to sleep (MSLT)

introspective - self-assessment of internal state (ESS, SSS)
SSS used as part of test of ongoing sleepiness

Manifest - behavioural signs of sleepiness, inability to volitionally stay awake, performance deficit on psychomotor or cognitive tasks (MWT, PVT)

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10
Q

Name two manuals used to classify disorders - what are the main cateogires

A
ICSD-2 
8 catorgies 
insomnia 
parasomnias 
sleep realted breating diorders 
Sleep related movement disorders 
Hypersomnias of central origin 
circadian rhythm sleep disorders 
isolated symptoms apparently normal variants &amp; unresolved issues 
other issues 
ICSD-3 
six categories 
Insomnia 
Sleep-related breathing disorders 
Central disorders of hypersomnolence 
Circadian rhythm sleep-wake disorders 
parasomnias 
sleep-related movement disorders 

DSM-5 sleep-wake disorders. 11 diagnostic groups

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11
Q

ICSD- 3 categories

A
Insomnia 
Sleep-related breathing disorders 
Central disorders of hypersomnolence 
Circadian rhythm sleep-wake disorders 
Parasomnias 
Sleep-related movement disorders
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12
Q

What is the multiple sleep latency test, and how does it help in the diagnosis of sleep disorders?

Why? 
Rationale 
How 
- series of nap oopurtunites X hours after awakening 
PSG measure sleep onset latency 
X to resist falling asleep 
PSG use XX 

Between tests what do they do?

How many tests - X-X
when? X hours apart

Terminated
XX mins after sleep onset - make sure they aren’t going into REM
if REM is before XX mins indicator of ———–
OR terminated when
– no sleep
clear sleep onset _x__ epochs of N1 and 1 of N2,N3 or REM

DIagnosing
—————- or i———– h—————–
treatments for b———— d————
sleep onset latency

A

determination of DTS –
People who are sleepier tend to fall asleep faster – due to (process S)

2 hours
PSG used to measure sleep onset latency (EEG, EMG and EOG)
not
Between tests subjects have to get out of bed
night before

• 4-6 tests performed, repeated every 2 hours
Terminated
15 mins after sleep onset – want to make sure they aren’t going into REM.
narcolepsy.
o 20 mins if no sleep
o Clear sleep onset – 3x30s epochs of n1 and one epoch of n2, n3 or REM)

Diagnosing: 
narcolepsy and idiopathic hypersomnia. 
Treatments for breathing disorders 
The time to sleep onset is averaged/ individual tests to give mean MSLT score 
< 8 mins are abnormal, 
<5 mins indicate severe EDS. 
Health adults = 10-20mins

Confound –
atypical sleep the previous night, hence PSG night before
Use of medications like stimulants or anti-depressants

Must consider other potential explanations, e.g. a fatigue condition.

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13
Q

What is the maintenance of wakefulness test, and how does it help in the diagnosis of sleep disorders?

What does it measure? 
Why? 
How? 
What do they measure? 
When is it terminated? 
N1 for - epochs or after -- mins 

How many times is it repeated?
after _ hrs - trials in total
During breaks patients patients can __ but they can’t go _______ because________

Diagnosis
ability to remain awake for __ = strongest evidence of normal altertness
sleep onset < _ mins = abnormal (longer than MSLT)
effectiveness of ______
evaluate the ____ of someon’s job involves public transport/safety - some occupations require a MWT to be conducted

A

measures manifest sleepiness.
stay awake may be more important to know than the ability to fall asleep.
Subjects instructed to stay awake dimly lit room, on a bed, with no additional activities such as reading or TV.
o Simultaneous PSG.
o terminated when clear unequivocal sleep occurs (at least N1, for 3 epochs) or after 40 minutes.
o Repeated after 2 hours, 4-5 trials in total.
o During breaks between trials, patients can watch TV, eat, read etc. but can’t go outside into the daylight.
 Ability to remain awake for the whole 40 mins = normal alertness,
 sleep onset < than 8 mins abnormal (longer than MSLT)
o Can be used to assess the effectiveness of CPAP
o Can also be used to evaluate risk if someone’s job involves public transport/safety – some occupations require an MWT to be conducted.

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14
Q

How might you investigate day time sleepiness? (physiological, Introspective, Manifest
Describe some sleep questionnaires

A

physiological
introspective
manifest

P = biological drive to sleep, measured by MSLT <5 mins = severe pathological HA= 10-15mins

I = sleep questionnaires, self-assessment of the internal state
ESS - chance of falling asleep in certain situations
SSS - over time level of alterness (may miss certain aspects of sleep)

M = behavioural signs of sleepiness, inability to volitionally stay awake performance defifict on cognitive tasks or psychomotor tasks 
Measures = MWT, PVT
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15
Q

Name two manuals used to classify disorders – what are the main categories in each manual

ICSD-2 - ICSD-3 (8 categories to 6 categories) 
I
SRBS
CDHy
CRD
P
SRMD
other 
DSM5 11 
I, 
Hy
Nar
OSA hyp
CSA
SRHv
CRSWD
NREM sleep arousal 
Nightmare 
REM SBD
RLS
A

• International classification of Sleep Disorders (ICSD-3) was simplified from ICSD-2 which had 8 categories, and has been condensed down to 6 major categories
o Insomnia,
 category is much shorter than ICSD-2 as all diagnoses characterised by a chronic insomnia disorder have been collapsed into a single diagnosis (chronic insomnia disorder)
o Sleep-related breathing disorders include OSA, CSA, sleep-related hypoventilation and sleep-related hypoxaemia.
o Central disorders of hypersomnolence include narcolepsy 1 and narcolepsy 2, Kleine-Levin syndrome (‘sleeping beauty syndrome’) etc.
o Circadian rhythm disorders include delayed and advanced sleep-wake phase disorder, shift work disorder, jet lag disorder etc.
o Parasomnias include sleep terrors, sleep walking, recurrent sleep paralysis, exploding head syndrome.
o Sleep-related movement disorders include PLM, RLS.
• ‘other sleep disorder’ and appendices for disorders and substance abuse which can have a secondary impact on sleep.

• DSM-5 sleep-wake disorders. 11 diagnostic groups:
Insomnia, hypersomnolence, narcolepsy, OSA hypopnea, CSA, sleep-related hypoventilation, circadian rhythm sleep-wake disorders, NREM sleep arousal disorders, nightmare disorder, REM sleep behaviour disorder, restless legs syndrome
• DSM-5 eliminated two previous diagnoses – sleep disorder related to another mental disorder, and sleep disorder related to another medical condition.

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16
Q

What is insomnia, what is it characterised by, what is the prevalence and how is it treated

What?
complaint of SL, SM, EA,NRS despite ao, and DTS
without DTS no diagnosis

Types: 
ASD 
PI 
PSyI
BIC 

ICSD simplies into X and X

Prevalence
Ohayon & Reynolds (2009)
X sectional study of –,— people –.-% reported at least one insomnia symptom -.-% met DSM-IV and approx -& ICSD
prevalence is depending on a– and g——
1/2 met diagnostic crtieria also met criteria for a m—- and a——- disorders are most common

MH association Jonhsonet al (2006)
I precede D
A precede I

Treatment = b————– safely adminseterd for _ weeks best when combined with —–
M——— sleep inducing aent

A

What complaint of sleep onset, sleep maintenance, early awakening, non-restorative sleep despite adequate opportunity to sleep and patients suffer day time impairment.
• Without day time impairment – individuals perceived need for treatment will not receive diagnosis of insomnia.

Adjustment sleep disorder
 Associated with specific stressor

Paradoxical insomnia
 Subjective report of severe sleeplessness not congruent with the absence or minor degree of daytime impairment
 Feel terrible but PSG = fine

Psychophysiological insomnia
 Working in bed
 Learned sleep preventing associations

Behavioural insomnia in childhood
 Inadequate limit setting

ICSD-3 simples into immediate and long-term insomnias

Ohayon and Reynolds (2009)
25,000
34.5% reported at least one insomnia symptom (6.6% met DSM-IV criteria and approx. 2% ICSD
age and gender
mood and anxiety disorders are most common

However, this was a sleep diary study asking coarse questions – despite large cohort

MH association supported by Johnson et al (2006)
 Insomnia precedes depression (3.8)
 Anxiety precedes insomnia (3.5)

Treatment: medication benzodiazepines can be safely and effectively administered for longer than three weeks most efficacious when combined with –
for short-term and chronic insomnia need behavioural intervention in form of sleep hygiene education, stimulus-control therapy and CBT
• Melatonin may also be used as sleep-inducing agents

17
Q

What is Fatal-familial Insomnia how does it differs from insomnia

What is it
what is it caused by - how does this differ from insomnia

progressive working memory attentionm ordering and frontal lobe functions

provides evidence for the necessiting of ____ sleep

CURE?
barbiturates —– the course of FFI

A

it is a transmissale prior diease
it is not a sleep disorder
mutated protien found in 40 familes world wide
It is fatal and leads to deat within 8-72 months a mean of 18 months

diagnosed around 50 yrs and therefore important for family planning 50% chance of inheritance

effects like insomnia
but the cause is due to a mutated protien PrP^C causing THALAMIC HYPOMETABOLISM and ATROPHY there are a lack of spindles and SWS but N1 is conserved
Insomnia may be caused by depression anixety or phyiscal healthconditions

deep - N1 clearly not sufficient for restoring the body

o FFI lack of a cure
o insomnia, treatments = CBT, good sleep hygiene, and sleeping medication.
 Sleeping medication such as barbiturates hasten the course of FFI

18
Q

What is narcolepsy

Prevalence 1/—-
HY

CAUSE 
abnormalities in the ---
--% carrying gene 
However only increase from of _-_% 
still a --/-- fold inc vs GP 

relation between O and N
O is a N—P——– confined to a small no of cells in the ——–
patients with N have often lost those o producing neruons
accroding to the / model uncontrollable passing between w and s state

CHARACTERISED 
DTS 
C
Hyp Hall
SP
AutBeh
DIAGNOSIS
(3 tests) 
P asses QoNS
M assess REM o and S
E asses sub DTS 

What is normally mistaken for
L
S
Poor SH

TREATMENT
Complete not poss
LA - S, N, SH

Zucconi and Ferri (2014)
Narcolepsy in ICSD-2 Narc w and Narc wo
/ T1 and T2
allowed patients w/o to be classfied with those who have c

A

Hypersomnia
rare neurological disorder affecting 1/2000 people

Cause:
ocentral nervous system
90%
1-2%. Still a 10-40-fold increase vs. general population.
Relation between hypocretin and narcolepsy –
neuropeptide confined to a small number of cells in the hypothalamus.
Patients with narcolepsy have often lost these orexin-producing neurons.
flip-flop
wake and sleep state

Characterised:
o Fall asleep inappropriately times in the day – particularly in non-stimulating activities despite adequate op to sleep night before
Other symptoms include:
o cataplexy (sudden & brief spells of muscle weakness) often triggered by emotional events
o Hypnagogic hallucinations – at sleep onset or offset
o Sleep paralysis
o Automatic behaviour
o Disrupted night-time sleep

Diagnosis
o Overnight PSG to assess quality of nocturnal sleep
o MSLT to assess REM onset and sleepiness
o ESS to assess DTS
Usually diagnosed in adolescence/young adulthood, mistaken for:
 laziness, depression, poor sleep habits.
 Can make it harder to get a diagnosis.

Treatment:
complete control of symptoms is not possible – medication helps EDS but not the condition itself
o Lifestyle alterations to manage stress, taking naps daily (10-15 mins) more basic sleep hygiene issues

Zucconi and Ferri (2014) – narcolepsy in ICSD-2 was defined as ‘narcolepsy with’ and ‘narcolepsy without’ cataplexy. Now, it’s been subdivided into type 1 and type 2. These changes allow patients without cataplexy, but with deficient hypocretin, to be classified together with those who have cataplexy.