MIDTERM Flashcards
(131 cards)
1
Q
Around 4% of the adult population experiences a level of daytime
sleepiness that could be considered abnormal and potentially
intrusive or even dangerous to routine daily activities.
A
EXCESSIVE DAYTIME SLEEPINESS
2
Q
Complaints of drowsiness or an appropriate and excessive
tendency to nap during the day need to be carefully distinguished
from simple:
A
tiredness
fatigue
Lack of energy
3
Q
Symptoms of EDS
A
Poor concentration
motor clumsiness
automatic behaviour
4
Q
EDS can still be dismissed by many as resulting merely from
A
poor lifestyle habits
laziness
reduced motivation
5
Q
These phenomena usually have different etiologies, such as chronic fatigue
syndrome in which there is no objective for an increased tendency to fall asleep.
A
EXCESSIVE DAYTIME SLEEPINESS
6
Q
Often mistakenly attributed to reflect mood disorder (depression),
hormonal balance (hypothyroidism) or anemia.
A
EXCESSIVE DAYTIME SLEEPINESS
7
Q
formal diagnosis of sleep disorder causing EDS may be delayed in youngsters
who display behavioral problems of irritability or paradoxical hyperactivity rather
than more obvious symptoms of sleepiness
A
EXCESSIVE DAYTIME SLEEPINESS
8
Q
Teenager and young adults, in particular, may seek to ‘
“ self-medicate” with
recreational stimulant drugs.
A
EDS
9
Q
The potential hazards of EDS when performing monotonous task such as
driving are obvious and often preventable.
A
EDS
10
Q
Occupational health physicians are increasingly aware of EDS as an issue both
at work and on the daily commute, especially in shift worker.
A
EDS
11
Q
usually a persistent or chronic
symptoms although there are a few rare causes of intermittent sleepiness,
A
EDS
12
Q
Primary sleep disorders
with sleep-wake dysregulation
A
Narcolepsy
*diopathic hypersomnolence
* Klein-Levine syndrome
13
Q
Circadian misalignment
A
Shift work sleep
disorder
* Jet lag
* Delayed sleep phase
syndrome
14
Q
Sleepiness secondary to a
chronic disorder
A
Obstructive sleep
apnoea/hypopnoea
syndrome
Restless legs syndrome
, Parkinson’s disease
* Depression
* Myotonic dystrophy
Multiple sclerosis
* Pain syndromes
15
Q
The commonest cause
of mild sleepiness
A
simply insufficient
nocturnal sleep.
16
Q
EDS can be broadly
divided into three
categories
A
Primary sleep disorders
with sleep-wake dysregulation
Sleepiness secondary to a
chronic disorder
Circadian misalignment
17
Q
most frequently starts in early adolescence and is a lifelong
affliction.
A
Narcolepsy
18
Q
This produces a deficiency of a neuropeptide
A
hypocretin
19
Q
a key regulator of the sleep-wake cycle.
A
hypocretin
20
Q
Has been recognized as a distinct syndrome for well over a century although it
is only in the last decade that its underlying neurobiology has been established
A
NARCOLEPSY
21
Q
Genetic analysis of a canine model of narcolepsy le to the surprising discovery
that classical cases of human narcolepsy arise from specific destruction of a few
thousand neurons in the lateral hypothalamus.
A
NARCOLEPSY
22
Q
Given its specific neurochemical basis, it is perhaps not surprising that there is a
spectrum of severity such that mild cases often escape medical attention.
A
NARCOLEPSY
23
Q
Irresistible sleep episodes, occasionally without recognizing the prior imperative
to sleep, may produce
A
“sleep attacks”
24
Q
Naps are typically fairly short and often refreshing.
A
(around 20 minutes or less)
25
Specific and diagnostically important symptom in narcolepsy
cataplexy.
26
Many narcoleptics can sustain wakefulness if engaged in alerting activities but
fight sleep if bored or unoccupied.
NARCOLEPSY
27
which full awareness is diminished
and automatic behaviors may occur with poor recall
"micro sleeps"
28
Attacks are generally brief and take a few seconds to build up
Typically with head bobbing or facial jerking at the onset.
This may suggest an epileptic phenomenon although a key feature of
cataplexy is maintained awareness of the environment even when paralyzed
29
may help to confirm clinical impressions and exclude
other diagnoses.
INVESTIGATIONS
30
International guidelines have rightly placed great emphasis on the presence of
typical cataplexy which, if present, in the context of EDS is sufficient for a
positive diagnosis.
INVESTIGATIONS
31
Many authorities, however, would advocate obtaining objective evidence of
sleepiness by ____________
undertaking a multiple latency test (MSLT)
32
Over four or five nap opportunities at two-hourly intervals, a narcoleptic should
fall asleep, on average, within eight minutes or sooner and enter REM sleep
within 15 minutes in at least two of the naps.
Over four or five nap opportunities at two-hourly intervals, a narcoleptic should
fall asleep, on average, within eight minutes or sooner and enter REM sleep
within 15 minutes in at least two of the naps.
33
Most narcoleptics benefits from drug medication although planned brief naps
during day or adjustments to diet can improve symptom control in many
Most narcoleptics benefits from drug medication although planned brief naps
during day or adjustments to diet can improve symptom control in many
34
Caffeinated drinks or caffeine supplements from pharmacies are rarely
sufficient to provide normal alertness but can be a useful supplement.
Caffeinated drinks or caffeine supplements from pharmacies are rarely
sufficient to provide normal alertness but can be a useful supplement.
35
It should be emphasized that, even with optimal drug treatment, a significant
proportion of patients are never normalized with respect to their sleep-wake
cycle.
It should be emphasized that, even with optimal drug treatment, a significant
proportion of patients are never normalized with respect to their sleep-wake
cycle.
36
usually the most disabling symptoms and combination of wake-promting
agents typically modafinil and dexamphetamine, may be needed.
EDS
37
may improve concurrently with increased wakefulness but
approximately 50% of patients benefits from additional medication.
Cataplexy
38
It is controversial drug, largely due to its commercial expense and fears over
potential misuse recreationally.
It is controversial drug, largely due to its commercial expense and fears over
potential misuse recreationally.
39
may therefore be justified in certain situations, particularly if
narcoleptic symptoms are atypical.
Brain imaging
40
With increasing knowledge of sleep neurobiology and the nature of narcolepsy,
it is valid to consider secondary causes especially if there is proven pathology in
the region of the hypothalamus.
SECONDARY NARCOLEPSY
41
Very occasionally, inflammatory disorders such as multiple sclerosis may be
associated with a form of narcolepsy with lesions seen in or around the
hypothalamus on imaging.
SECONDARY NARCOLEPSY
42
A variety of structural pathologies in the region of the floor of the third ventricle,
adjacent to the hypothalamus, have also been reported to cause narcoleptic
symptoms.
SECONDARY NARCOLEPSY
43
In a range of neurological disorders, the level and nature of EDS may mimic
narcolepsy even if the underlying mechanism remains obscure.
SECONDARY NARCOLEPSY
44
Examples include myotonic dystrophy, Parkinson's disease, head injury and
certain rare developmental disorders, such as Prader- Willi syndrome
SECONDARY NARCOLEPSY
45
A rare cause of severe EDS often affecting young populations and potentially
mimicking narcolepsy
IDIOPATHIC HYPERSOMNOLENCE
46
The underlying neurobiology is not established and subjects simply appear to
need far more sleep than average.
IDIOPATHIC HYPERSOMNOLENCE
47
In typical cases, despite 10 hours of good quality sleep, there are major
difficulties arising at a conventional hour and a subsequent propensity for
prolonged unrefreshing daytime naps.
IDIOPATHIC HYPERSOMNOLENCE
48
Unlike narcolepsy, there are few symptoms suggesting abnormal REM sleep or
related phenomena.
IDIOPATHIC HYPERSOMNOLENCE
49
In some patients the clinical picture appears to lie between IH and narcolepsy.
IDIOPATHIC HYPERSOMNOLENCE
50
In general wake-promoting treatment tend to be less successful in IH, with
many patients unable to work or study effectively.
IDIOPATHIC HYPERSOMNOLENCE
51
Frustration and depression are frequent associations.
IDIOPATHIC HYPERSOMNOLENCE
52
Symptoms typical in IDIOPATHIC HYPERSOMNOLENCE
1Unavoidable daytime naps
2Automatic behaviours common
3Overnight sleep is prolonged
4Morning waking difficult
5Sleep latency is around eight
minutes or less on a multiple
sleep latency test (MSLT)
Mood disorder common
53
Naps tend to be long and unrefreshing
but otherwise unremarkable (e.g. no
dream phenomena)
Unavoidable daytime naps
54
There is usually reduced alertness
throughout the day such that some
behaviours are performed on
*autopilot and not recalled
Automatic behaviours common
55
Sleep quality and quantity appear
normal or even better than average
when formally measured by
investigations
Overnight sleep is prolonged
56
Often the most disabling symptom
with subjects appearing 'confused' or
irritable if awoken at a conventional
hour
Morning waking difficult
57
If present, this probably is more likely
a consequence rather a cause of the
excessive sleepiness
Mood disorder common
58
In a 20-minute nap opportunity,
subjects with IH usually fall into deep
non-REM sleep but not REM sleep
Sleep latency is around eight
minutes or less on a multiple
sleep latency test (MSLT)
59
Primary chronic insomnia almost certainly has long-term health consequences
and is strongly associated with depression, hypertension and a variety of physical
or somatic symptoms
Primary chronic insomnia
60
most commonly precipitated by a trigger or life event in
predisposed subjects and is subsequently fulled over months or years by
maladaptive thoughts and habits
Chronic insomnia
61
most cases of primary insomnia and
is thought primarily to reflect excessive cognitive arousal
Psychophysiological insomnia
62
best
proven treatment for severe or resistant cases.
Structured cognitive behavior therapy
63
Acute insomnia lasts from 1 night to a few
weeks.
Acute insomnia
64
Insomnia is chronic when it happens at least 3 nights a week for 3
months or more
chronic
65
usually triggered by a recognizable life event
or stressor. It is universally recognized phenomenon.
Transient or short-term insomnia,
66
recognized as a reliable independent risk factor for developing
depression and hypertension.
Insomnia
67
MECHANISM OF INSOMNIA:
Four Interacting Factors that can contribute to insomnia in Clinical
Practice
1Homeostatic Factors
2MALADAPTIVE COPING MECHANISMS AND BEHAVIOURS
3STRESS RESPONSE
4STRESS HYGIENE
68
If sleep drive is weak' for some reason or, perhaps more commonly , if
someone is overly aroused or wakeful, insomnia may result.
Homeostatic Factors
69
Many potentially reversible behaviors, habits or beliefs exist to promote or
worsen insomnia.
MALADAPTIVE COPING MECHANISMS AND BEHAVIOURS
70
The increased reactivity may be compounded by any underlying anxiety or
mood disorder.
STRESS RESPONSE
71
A central tenet of any treatment for insomnia is the concept of good sleep hygiene
STRESS HYGIENE
72
highly recommended in those prone to
insomnia
A consistent sleep-wake schedule
73
Commonest form of primary insomnia, reflecting an interaction
psychological
and physical factors.
74
accounts for most cases of primary insomnia and
is thought primarily to reflect excessive cognitive
Psychophysiological insomnia
75
some subjects sleep particularly badly if
closely monitored overnight where areas others find they sleep more easily when
away from their normal bedroom environment.
polysomnography,
76
is occasionally used to explore sleep-wake cycles at home over
a period of weeks, particularly if there are suspicious of paradoxical insomnia.
Wrist actigraphy
77
should be simple, possibly using a graphical format over 24 hrs
diary
78
can be very useful in identifying and monitoring progress in
insomnia patients in whom there is poor sleep hygiene or inappropriate
scheduling.
Sleep diaries or logs
79
designed to encourage peaceful
thoughts and release muscle tension are widely available.
Reading materials or audio tapes
80
A typical structured six-week CBT programme for
insomnia
Week 1 detailed assessment and measurement of the insomniaproblem;definition of realistic goals of treatment
Week 2 education on sleep and its function with particular
reference to insomnia
Week 3 sleep hygiene and relaxation
Week 4 scheduling a new sleep pattern
Week 5 dealing with a racing mind and unhelpful thoughts
Week 6 putting it all together
81
used as surrogate hypnotic agents even though
overall sleep quality is often not improved due to their adverse of inhibitory effects on
deep non-REM sleep
sedative drugs
82
If sleep onset is the main complaint., the lowest dose of a short-acting drug
Zolpidem,
83
If sleep maintenance is the major
concern,
as Zopiclone or temazepam
84
available as long a long-acting preparation licensed for use in primary
insomnia.
Melatonin
85
only central derivations were used to stage
sleep, the term "movement time" was utilized to characterize
epochs in which the electroencephalographic (EEG) and eye
movement tracings are obscured by patient movement, and there
wast a 3-minute rule for the continuation of stage.
the R&K manual,
86
sleep was staged according to the manual
Rechtschaffen and Kales (R&K) 1968 to 2007,
87
The AASM scoring manual continues the convention of
staging sleep in sequential 30-second epochs.
The AASM scoring manual continues the convention of
staging sleep in sequential 30-second epochs.
88
assigned a sleep stage.
epoch
89
patients make the
transition from full alertness to the early
stages of drowsiness.
wakefulness,
90
the EEG consists of
low-amplitude activity (chiefly beta and
alpha frequencies) without the
rhythmicity of alpha rhythm (8-13 Hz
most prominent over occipital
derivations).
eyes open stage W,
91
SEMs may or may not be present during
periods when alpha rhythm is present.
STAGE W
RULE
92
In subjects who generate alpha rhythm,
stage W is scored when more than 50% of
the epoch contains alpha rhythm over
the occipital region.
STAGE W
RULE
93
A 30-second
epoch in which no sleep
spindles or K complexes
are noted in the
electroencephalogram
(EEG). Less than 50% of
the epoch has alpha
rhythm.
Stage N1.
94
is characterized by the presence of one or more nonarousal
KCs (i.e., KCs NOT associated with an arousal) or one or more trains of
SSs. Arousal rules are discussed later in this chapter.
Stage N2
95
said to be associated with an arousal (KC+Ar) if the
arousal commences no more than 1 second after the termination of the
KC.
KC
96
IVIAUUR DIALLY ARLAD
IMPORTANT FOR SLEEP AND®
WAKE
HYPOTHALAMIC AREAS
97
Histaminergic neurons are confined to the posterior hypothalamus in the area
called the tuberomammillary nucleus.
tuberomammillary nucleus.
98
project to the cerebral cortex, amygdala, substantia nigra (SN),
DRN, LC, and nucleus of the solitary tract.
TMN neurons
99
associated with wakefulness, and antihistamines
(H1 receptor blockers) cause drowsiness or sleep.
HA acting at H1 receptors
100
The TMN receives stimulatory input from the
lateral hypothalamus
101
is defined as movement and muscle artifact obscuring the
EEG for more than half an epoch to the extent that the sleep stage cannot be determined.
major body movement (MBM)
102
the amount of
SWA (SWA = EEG activity
of 0.5-2 Hz and a peak-to-
peak amplitude of > 75 Mv
measured over the frontal
areas) is equal to or
greater than 20% of an
epoch (≥6 sec).
stage N3,
103
The EEG activity in stage R resembles that of stage N1 and generally contains
LAMF activity. However, alpha activity in V stage R is usually more prominent
than in stage Nl and usually has a frequency 1 to 2 Hz lower than during
wakefulness.
STAGE R
104
The three components of stage R are
(1) a low-amplitude EEG without KCs or SSs,
(2) REMs
(3) low chin EMG tone (activity)
105
When epochs have all three ite
or unambiguous epochs of REM
sleep. The EEG has low amplitude mixed frequency activity, REMs are present, and
chin EMG tone is low.
REM SLEEP (REM RULE
106
transient phenomenon that may lead to wakefulness or only
briefly interrupt sleep. They are worth scoring because patients with
frequent arousals may have daytime sleepiness even if the total sleep
duration is normal.
Arousals
107
tend to
increase REM sleep, and serotonergic medications tend to impair sleep
cholinergic medications
108
general cause sleepiness,
antihistamines
109
scoring Manual,
provides new scoring rules for infants older than 2 months and
children.
The American Academy of Sleep Medicine (AASM)
110
sleep was staged
according to the sleep scoring rules of
Anders, Emde, and Parmelee.
111
using frontal (F3, F4, FT, F8), central
(C3 and C4), parietal (P3, P4, P7, and P8), and occipital (O1 and 02)
electrodes.
using frontal (F3, F4, FT, F8), central
(C3 and C4), parietal (P3, P4, P7, and P8), and occipital (O1 and 02)
electrodes.
112
montages are illustrated using frontal (F3, F4, FT, F8), central
(C3 and C4), parietal (P3, P4, P7, and P8), and occipital (O1 and 02)
electrodes. Some of these electrodes are used in standard sleep
recording and others are not.
bipolar electroencephalogram
113
Infant sleep is divided into
active sleep
sleep), quiet sleep
indeterminant sleep,
114
The EEG patterns of sleep in the pre-term and term
infant are
Tracé discontinue
Tracé alternant
3. Low-voltage irregular
115
discontinuous pattern consisting
of high-voltage bursts with sharp features separated by long,
dramatically flat EEG periods of 10 to 20 seconds TD is seen at or before
30 weeks and is the EEG pattern of QS in that age group.
Tracé discontinue
116
A discontinuous pattern that characterizes the
QS of newborns after about 30 weeks CA. Bursts of mixed activity of 2 to
8 seconds are interspersed with periods of flatter EEG. The bursts are
composed of high-voltage slow waves superimposed with rapid low-
voltage sharp waves
Tracé alternant
117
Continuous low-voltage mixed-frequency
with prominent delta and theta rhythms and little variation. Voltage (14-
35 M V), theta rhythm predominates
3. Low-voltage irregular (LVI):
118
& Newborn infants typically have periods of sleep lasting 3 to 4 hours
interrupted by feeding, and the total sleep duration in 24 hours is usually 16
to 18 hours.
SLEEP ARCHITECTURE
119
The following terminology should be used when scoring
sleep in children 2 months postterm or older:
Stage W (wakefulness)
2. Stage N1 (NREM 1)
3. Stage N2 (NREM 2)
4. Stage N3 (NREM 3)
5. Stage N (NREM)
6. Stage R (REM)
120
is defined as the predominant rhythm seen over occipital derivations during eyes
closed wakefulness that is reactive. (Reactive = activity blocks or attenuates with eye
opening and appears with passive eye closure.)
DOMINANT POSTERIOR RHYTHM
121
The PR in adults
"alpha rhythm"
122
This waveform
occurs in children between 8 and 14 years and has a frequency of 2.5 to 4.5 Hz.
PSW usually occurs at the same time as DPR with eyes closed wake and
disappears with drowsiness or transition to stage N1 sleep. Maximal incidence
is 8 to 14 years of age, rare younger than 2 years or
Posterior slow waves (PSWs) of youth:
123
Eye blinks in children, as in adults, are associated
with the eyeball turning upward (Bell's phenomenon). In
children, they cause occipital sharp waves that are monophasic or biphasic
(200-400 msec) and less than 200 Mv that follow eye
Blinks:
124
3. Slow eye movements (SEMs) or REMs are defined the same as in adults.
3. Slow eye movements (SEMs) or REMs are defined the same as in adults.
125
WAVEFORMS FOR SCORING PEDIATRICS N1
Rhythmic anterior theta (RAT)
Hypnagogic hypersynchrony (HH)
Low-amplitude mixed-frequency (LAMF):
Vertex sharp waves
SEMs:
126
activity consists of runs of moderate
voltage, 5- to 7-Hz, activity largest over thefrontal regions. RAT activity is
common in adolescents and young adults during drowsiness and first
appears around 5 years of age
Rhythmic anterior theta (RAT)
127
is characterized by bursts of very high
amplitude 3- to 4.5-Hz sinusoidal waves maximal in frontal and central
derivations and smallest in the occipital derivation (widely distributed)
Hypnagogic hypersynchrony (HH)
128
Lowamplitude, predominantly
4- to 7-Hz activity.
Low-amplitude mixed-frequency (LAMF):
129
sharply contoured waves with duration less than
0.5 second maximal over the central region and distinguishable from
background activity.
Vertex sharp waves
130
Conjugate, reasonably regular, sinusoidal eye movements with
initial deflection that last longer than 500 msec.
SEMs:
131
If alpha/DPR is not generated, score stage N1 commencing
with the earliest of any of the following
phenomena:
1. Activity in range 4 to 7 Hz with slowing of background frequencies by 1 to 2 Hz or
higher from
stage W (e.g., 5 Hz and stage W had 7 Hz).
2. SEMs.
3. Vertex sharp wave,
4. RAT activity.
5. HH.
6. Diffuse or occipital predominant high-amplitude rhythmic 3- to 5-Hz activity.
