Sleep in Other Disorders Flashcards
1
Q
What is ALS?
A
A progressive motor neuron disease with a poor prognosis
2
Q
What are the main characteristics of ALS?
A
Progressive limb, bulbar, and respiratory muscle weakness leading to death
3
Q
How can the survival and quality of life of patients with ALS be improved?
A
With a multidisciplinary approach including respiratory support with NIV and airway clearance interventions
4
Q
In ALS patients, when are nocturnal desaturation and hypoventilation most prominent?
A
During REM sleep due to muscle paralysis combined with diaphragmatic weakness
5
Q
What FVC value qualifies a patient for NIV?
A
FVC <50% or inability to generate a maximal inspiratory pressure of -60 cm H2O in the absence of lung disease
6
Q
Is a sleep study required to initiate NIV in patients with progressive neuromuscular disease?
A
No, a sleep study is not required
7
Q
What are the mainstays of treatment for ALS patients requiring NIV?
A
Volume or pressured cycled NIV
8
Q
What is the recommended duration of NIV use for better outcomes?
A
> 4 hours per day
9
Q
What effect does NIV have on FVC decline in ALS patients?
A
Slows the decline in FVC
10
Q
Does NIV improve sleep efficiency or decrease arousals in ALS patients?
A
No, it does not improve sleep efficiency or decrease arousals
11
Q
What is the survival benefit of using NIV for >4 hours per day in ALS patients?
A
7-month survival benefit compared to those using it <4 hours per day
12
Q
What is the effect of NIV on oxygen saturation during sleep in ALS patients?
A
NIV improves oxygen saturation
13
Q
Is autotitrating bilevel pressure ventilation recommended for ALS patients?
A
No, it is not recommended
14
Q
True or False: NIV improves survival in all ALS patients, including those with severe bulbar involvement.
A
False
15
Q
What may result from maxillary constriction?
A
Greater nasal resistance and mouth breathing
This can also lead to retroglossal airway narrowing, increasing the likelihood and severity of obstructive sleep apnea (OSA).
16
Q
What is RME an abbreviation for?
A
Rapid Maxillary Expansion
RME is an orthodontic technique used to widen the upper jaw.
17
Q
What primary benefit does RME provide?
A
Reduces nasal resistance
This is particularly important when the upper jaw is too narrow.
18
Q
Is orthognathic surgery alone sufficient for severe OSA?
A
No
It may not be sufficient without complementary procedures.
19
Q
What conventional surgeries can RME complement?
A
- Adenotonsillectomy
- Maxillary-mandibular advancement
These surgeries are typically used for treating OSA.
20
Q
What does rapid maxillary expansion typically involve?
A
- Maxillary or maxillomandibular transverse distraction osteogenesis
- Orthodontic alignment and leveling
This approach is aimed at enhancing facial morphology and dental occlusion.
21
Q
What anatomical changes are associated with RME?
A
- Increases lateronasal width
- Increases pyriform opening
- Increases intermolar distance
- Changes hyoid-to-mandibular plane distance
These changes can have beneficial effects on airway dynamics.
22
Q
What improvements have been noted in patients after RME treatment?
A
- AHI
- Snoring
- Oxygen saturation
- Hypersomnolence
These improvements have been observed in children, adolescents, and adults.
23
Q
How long do the beneficial effects of RME last?
A
2 years after treatment
This indicates that the effects can be sustained over a significant period.
24
Q
What percentage of young adults had a normal AHI after RME?
A
70%
This statistic reflects a successful outcome in improving sleep apnea metrics.
25
What improvements did RME produce in sleep architecture?
* Longer sleep period time
* Reduced number of stage shifts
## Footnote
However, sleep microstructure may not completely normalize.
26
True or False: Sleep microstructure completely normalizes after RME.
False
## Footnote
This highlights the need for long-term follow-up in patients.
27
OHS
28
29
What is overlap syndrome?
Overlap syndrome is defined as a combination of COPD and OSA, with symptoms usually worse than expected with either condition alone.
30
What is required for the diagnosis of obesity hypoventilation syndrome (OHS)?
The definition of OHS requires that no other major coexisting disease may account for the hypercapnia present.
31
Who coined the term 'overlap syndrome'?
Overlap syndrome was first coined by Flenley.
32
What symptoms should one beware of in an obese patient according to Flenley?
Beware the obese patient who snores, has COPD, and morning headaches.
33
How does overlap syndrome affect nocturnal hypoxemia?
Overlap syndrome usually causes more severe nocturnal hypoxemia than either disease alone.
34
What mechanisms did Flenley propose for nocturnal oxygen desaturation?
Flenley proposed mechanisms including alveolar hypoventilation, decreased ventilation-perfusion matching, and decreased end-expiratory lung volume.
35
What effect can oxygen therapy have on patients with overlap syndrome?
Patients may develop worsening hypercapnia with initiation of oxygen therapy.
36
What was the outcome of the randomized control trial of nocturnal bilevel PAP therapy in patients with severe COPD?
The trial showed benefit in reducing daytime hypercapnia in patients with severe COPD fulfilling the diagnosis of overlap syndrome.
37
What is the mortality rate for patients with overlap syndrome who are adherent to CPAP therapy?
Studies reveal a decreased mortality rate in patients with overlap syndrome who are adherent to CPAP therapy alone.
38
What does the oximetry tracing in overlap syndrome typically show?
The oximetry tracing shows reduced mean saturation and prolonged periods of saturation <90%.
39
What is associated with the characteristic marked worsening during REM sleep stage?
Deep clustered episodes of desaturation are associated with the marked worsening seen during REM sleep stage.
40
What is the prevalence of sleep apnea in patients with acromegaly?
Sleep apnea is common in patients with acromegaly; it is reported in >60% of such patients.
41
What type of sleep apnea is most common in patients with acromegaly?
The majority of patients with acromegaly and sleep-disordered breathing have obstructive sleep apnea (OSA).
42
What is the rate of central sleep apnea (CSA) in patients with acromegaly?
There is a higher rate of central sleep apnea (CSA) at 34%.
43
What may cause central sleep apnea in patients with acromegaly?
CSA is likely a manifestation of abnormal respiratory control, possibly related to abnormalities in the central somatostatin pathway or growth hormone effects on metabolic rate.
44
What anatomical changes contribute to increased OSA in patients with acromegaly?
Enlargement of the soft palate and macroglossia contribute to the increased OSA in these patients.
45
What factors increase the risk of sleep apnea in patients with acromegaly?
Many patients are overweight or obese, and factors like female sex, smoking, and underlying lung disease also correlate with a greater likelihood of sleep apnea.
46
What is the relationship between the pituitary mass and respiratory control in acromegaly?
Most features of acromegaly are attributed to the pituitary mass, but the mass itself does not have a direct impact on respiratory control.
47
How do surgical and medical interventions for acromegaly affect sleep apnea?
Both surgical and medical interventions for acromegaly have been shown to improve sleep apnea, but up to 40% of those with OSA may have persistent sleep apnea.
48
What are the GH and IGF-1 levels in patients with acromegaly and central sleep apnea?
Patients with acromegaly with central sleep apnea have significantly higher IGF-1 and GH levels than those with OSA.
49
What percentage of women developed RLS during pregnancy according to studies?
13% to 34% of women developed RLS during their pregnancy.
50
What happens to RLS symptoms after delivery?
Symptoms generally resolve within a few days after delivery.
51
What is the risk associated with pregnancy-related RLS?
Pregnancy-associated RLS significantly increases the risk for subsequent development of chronic idiopathic RLS.
52
How does the prevalence of RLS differ between men and women?
Women describe symptoms of RLS about twice as often as men.
53
What accounts for the difference in RLS prevalence between sexes?
Transient pregnancy-associated RLS accounts for much of the difference in prevalence noted between sexes.
54
In which group of women is RLS more prevalent?
RLS is more prevalent among parous women compared to nulliparous women, especially with a family history of the disorder.
55
What is likely to happen to women with prior pregnancy-associated RLS in future pregnancies?
Symptoms are more likely to reappear in women who have had prior pregnancy-associated RLS.
56
During which trimester is RLS most severe?
RLS occurs exclusively, or is most severe, during the third trimester of pregnancy.
57
What is the typical resolution time for RLS symptoms after delivery?
The majority of women experience complete resolution of RLS symptoms within a few days of delivery.
58
What are some reported risk factors for pregnancy-associated RLS?
Risk factors include a family history of RLS, past childhood growing pains, and multiple pregnancies.
59
What correlations have been suggested in some studies regarding RLS?
Some studies suggest a correlation with anemia, reduced serum folate, high estrogen and progesterone levels during pregnancy, smoking, and alcohol use.
60
Has iron or folate supplementation been shown to be effective for pregnancy-related RLS?
Iron or folate supplementation has not been consistently shown to be effective for pregnancy-related RLS.
61
What should pregnancy-associated RLS be distinguished from?
Pregnancy-associated RLS should be distinguished from leg cramps, essential tremor, tic disorder, dystonia, or tremors related to neurologic disorders.
62
What symptoms may lead patients to seek treatment for RLS?
Patients may seek treatment due to significant insomnia, sleep disturbance, excessive daytime sleepiness, or depressed mood.
63
Are pramipexole and ropinirole recommended for use during pregnancy?
Neither pramipexole nor ropinirole is currently recommended for use during pregnancy.
64
What is the FDA pregnancy category for pramipexole and ropinirole?
Both agents are considered FDA pregnancy category C.
65
What alternative treatments may be tried for pregnancy-associated RLS?
Local application of heat or massage may be tried.
66
What are TRDs?
TRDs are monobloc oral appliances designed to treat OSA by securing the tip of the tongue to a negative-suction cup over the front teeth.
67
What benefits do TRDs provide?
TRDs decrease snoring, subjective daytime sleepiness, and arousals; improve quality of sleep; and increase oxygen saturation during sleep.
68
In which patients is the therapeutic efficacy of TRDs greater?
The therapeutic efficacy is greater in patients with predominantly supine sleep compared to nonpositional OSA.
69
How do TRDs compare to MAS in terms of effectiveness?
TRDs are generally less effective in improving apnea-hypopnea indices than MAS.
70
How do TRDs and MAS compare to soft palate lifters?
Both MAS and TRDs are more effective than a soft palate lifter for the treatment of OSA.
71
What is a key preference among patients regarding oral appliances?
Patients tend to prefer MAS to TRD.
72
What has the US FDA approved regarding TRDs?
The US FDA has approved some TRDs as treatment for snoring and sleep apnea.
73
Who are TRDs useful for?
TRDs are useful for patients who prefer oral appliances to PAP therapy but cannot use MAS due to inadequate dentition or significant temporomandibular joint disorder.
74
What anatomical changes do TRDs and MAS cause?
Both TRD and MAS displace the parapharyngeal fat pads away from the airway and increase the velopharyngeal dimensions, but the pattern and extent of changes differ.
75
Do TRDs require adjustments?
TRDs require no adjustments and cost less than MAS.
76
What are the long-term adherence rates for TRDs?
Some studies have reported long-term adherence rates for TRDs greater than 50%.
77
What factors negatively affect compliance with TRDs?
The presence of nasal obstruction and the severity of dental occlusion negatively affect compliance.
78
How does dental occlusion affect compliance with TRDs?
Compliance is greater in patients with class 1 occlusion compared to those with class 2 or 3 occlusions.
79
How does compliance with TRDs compare to MAS?
Compliance is generally poorer for TRDs compared with MAS.
80
What are some complications of TRDs?
Complications of TRDs include soreness or elongation of the tongue.
81
What should sleep specialists be aware of regarding daytime fatigue and sleepiness?
Sleep specialists should be aware of medical conditions that constitute the differential diagnosis for daytime fatigue and sleepiness.
82
What types of conditions may mimic sleep disorders?
Endocrinologic and metabolic conditions such as Addison disease, hypothyroidism, hypercalcemia, and diabetes mellitus may manifest symptoms that mimic sleep disorders.
83
What symptoms did the patient with Addison disease present?
The patient presented with fatigue, salt craving, polyuria, polydipsia, low BP, and lack of sleepiness despite significant levels of fatigue.
84
What sleep issues can occur in patients with Addison disease?
Difficulty initiating and maintaining sleep with normal Epworth sleepiness scale scores has been described in patients with Addison disease.
85
What is suggested about cortisol secretion and slow-wave sleep?
Normal cortisol secretion is needed for the maintenance of slow-wave sleep.
86
How does fatigue in myasthenia gravis differ from that in Addison disease?
Fatigue in myasthenia gravis is better in the morning and worsens during the day, while in Addison disease, fatigue does not show diurnal variation.
87
How can myasthenia gravis be diagnosed?
Myasthenia gravis can be diagnosed by measuring antibodies to acetylcholinesterase in the serum and by improvement in pulmonary function testing following IV edrophonium administration.
88
What is high-altitude periodic breathing (HAPB)?
HAPB is characterized by cyclic central apneas and hyperpneas during sleep associated with ascension to altitude, resulting in sleep disruption and episodic nocturnal dyspnea.
89
What is the most effective method of preventing altitude-related illness?
The most effective method is to gradually ascend to the target elevation.
90
What should be done if gradual ascent is not possible?
If gradual ascent is not possible, acetazolamide should be started 24 to 48 hours before ascent.
91
Who should receive prophylaxis for altitude-related illness?
Prophylaxis is reserved for those at risk for altitude-related illness, particularly those with a prior history or those with cardiopulmonary disease.
92
What stimulates ventilation during sleep?
Hypoxemia stimulates ventilation, which is further destabilized during the sleep state.
93
At what altitude does HAPB typically occur?
HAPB typically does not occur at altitudes < 2,000 m.
94
What are common symptoms of HAPB?
Symptoms include repeated awakenings from sleep, a sense of dyspnea, and fatigue related to poor sleep quality.
95
What more severe features might accompany acute mountain sickness (AMS)?
More severe features of AMS might include headaches, fatigue, and nausea.
96
What are life-threatening forms of AMS?
Life-threatening forms of AMS include high-altitude cerebral edema and high-altitude pulmonary edema.
97
What is the drug treatment of choice for cerebral edema?
Dexamethasone is considered the drug treatment of choice for cerebral edema but is not indicated for HAPB.
98
What role do vasodilators like nifedipine play at high altitude?
Vasodilators, such as nifedipine, may help prevent pulmonary edema at high altitude but have no role in periodic breathing prevention.
99
How might acetazolamide help at high altitude?
Acetazolamide may have a role in preventing pulmonary edema, possibly through effects on calcium channels.
100
What is the effectiveness of hypnotics like zolpidem for HAPB?
Hypnotics, such as zolpidem, may be effective for insomnia related to travel but have not been shown to prevent HAPB.
101
What is nocturnal motor activity during sleep generally attributed to?
Nocturnal motor activity during sleep is generally thought to be due to a parasomnia or to seizure activity.
102
What is key for making the correct diagnosis of nocturnal motor activity?
Recognition of motor activity pattern on a video polysomnography recording is key for making the correct diagnosis.
103
What characterizes episodes of motor activity with NFLE?
Episodes of motor activity with NFLE are stereotypically rapid and sudden motor behaviors involving a body part or the whole body, which could be dystonic.
104
What age group do NREM parasomnias usually affect?
NREM parasomnias usually account for polymorphic nocturnal motor activity, mainly at a younger age.
105
When do NREM parasomnia attacks typically occur?
NREM parasomnia attacks typically occur out of slow-wave sleep, predominantly in the first part of the sleep period.
106
How long do NREM parasomnia attacks usually last?
Attacks usually last less than 1 minute.
107
What is the typical outcome of NREM parasomnias after puberty?
NREM parasomnias typically disappear after puberty.
108
When does NFLE typically show onset?
NFLE shows a later onset, in the second decade of life.
109
How do NFLE events differ from NREM parasomnia events?
NFLE events emerge from NREM sleep but occur throughout the sleep period and are not confined to slow-wave sleep.
110
How long do attacks of NFLE usually last?
Attacks of NFLE usually last for a few minutes.
111
What is the EEG finding in NREM parasomnia and NFLE?
EEG is normal in NREM parasomnia and can be normal in NFLE during and between attacks; therefore, EEG does not serve as a definitive diagnostic tool.
112
Is there a hereditary component to arousal parasomnia and NFLE?
Both arousal parasomnia and NFLE may have a hereditary component.
113
What percentage of patients with parasomnia had a brief arousal behavior preceding motor activity?
In one patient series, a brief arousal behavior preceded the motor activity in 80% of patients with parasomnia.
114
What percentage of patients with NFLE had a brief arousal behavior preceding motor activity?
In one patient series, a brief arousal behavior preceded the motor activity in 50% of patients with NFLE.
115
Are patients with parasomnia usually aware of their episodes?
Patients with parasomnia are not usually aware of the episodes.
116
Are patients with NFLE aware of their episodes?
Patients with NFLE are aware of the episodes and usually complain of sleep disruption and daytime sleepiness.
117
What is Fatal familial insomnia (FFI)?
FFI is a rare autosomal dominant prion disease characterized by a mutation at codon 178, thalamic damage, and insomnia.
118
What mutation is associated with FFI?
The mutation at codon 178 is associated with FFI.
119
What other disease shares the same mutation at codon 178 as FFI?
The familial form of Creutzfeldt-Jakob disease shares the same mutation at codon 178.
120
What distinguishes the mutated alleles at codon 129 for FFI and Creutzfeldt-Jakob disease?
In FFI, the mutated allele codes for methionine, while in Creutzfeldt-Jakob disease, it codes for valine.
121
What are the general characteristics of prion diseases?
Prion diseases are associated with the accumulation of abnormal isoforms of the prion protein in neurons, leading to apoptosis and cell death.
122
What is the average age of onset for FFI?
The average age of onset for FFI is about 50 years.
123
What is the typical duration of FFI?
The duration of FFI ranges between 7 and 36 months.
124
What are common symptoms of FFI?
Symptoms include sleep disturbance, hallucinations, delirium, and dysautonomia preceding motor and cognitive deterioration.
125
What is the irregular sleep-wake rhythm disorder?
It is characterized by a loss of the circadian pattern of sleep and wakefulness with no known familial pattern.
126
What is REM sleep behavior disorder?
It involves loss of muscle atonia with limited evidence for familial patterns.
127
What are essential features of FFI according to the International Classification of Sleep Disorders?
FFI is progressive, characterized by initial difficulties in falling asleep, spontaneous lapses into sleep with enacted dreams, and loss of slow-wave sleep.
128
What happens in the later stages of FFI?
Identification of distinct sleep stages may become difficult, and cognitive function is retained until impaired alertness makes testing impossible.
129
What is the final progression of FFI?
The disorder progresses to unarousable coma and finally death.
130
What associated features are present in FFI?
Associated features include bronchopulmonary infections, loss of diurnal/circadian endocrine rhythms, and autonomic hyperactivity.
131
What autonomic hyperactivity symptoms are present in FFI?
Symptoms include pyrexia, salivation, hyperhidrosis, tachycardia, tachypnea, and dyspnea.
132
What somatomotor disturbances are included in FFI?
Disturbances include dysarthria, dysphagia, tremor, myoclonus, dystonic posturing, ataxia, and a positive Babinski sign.
133
What diagnostic tool can support the diagnosis of FFI?
PET studies can provide support for the FFI diagnosis, such as midbrain hypometabolism.
134
What provides the final conclusive diagnosis of FFI?
Histopathology provides the final conclusive diagnosis.
135
What is stridor?
Stridor is a loud, high-pitched, inspiratory noise created by laryngeal or tracheal muscle dysfunction, resulting in complete or near-complete airflow cessation.
136
What may happen to individuals experiencing stridor during sleep?
Individuals may be unaware of its occurrence or may awaken with a feeling of panic.
137
How can stridor episodes be diagnosed?
Audio recording of episodes by a caregiver may assist in diagnosis.
138
What diagnostic tool is useful for assessing structural lesions in stridor?
Laryngoscopy is useful in assessing for structural lesions and to characterize vocal cord dysfunction.
139
In which condition is sleep-related stridor common?
Sleep-related stridor is common in people with multiple system atrophy (MSA).
140
What percentage of people with MSA experience sleep-related stridor?
Sleep-related stridor occurs in 12% to 42% of people with MSA.
141
What is the neurodegenerative disorder associated with alpha-synuclein deposition?
Multiple system atrophy (MSA) is caused by alpha-synuclein deposition within glial cells of the central nervous system.
142
How is probable MSA diagnosed?
A diagnosis of probable MSA is made on clinical grounds based on autonomic failure and either parkinsonism or cerebellar dysfunction.
143
What imaging techniques can be useful in unclear MSA diagnoses?
Neuroimaging with brain MRI, FDG-PET, or single-photon emission computed tomography can be useful.
144
What is the relationship between stridor and mortality in MSA?
Several studies have shown an association between stridor within 3 years of onset of MSA symptoms and earlier mortality.
145
What are the treatment options for sleep-related stridor?
Sleep-related stridor can be treated with CPAP or tracheostomy, with CPAP considered first line.
146
When is tracheostomy indicated for stridor?
Tracheostomy is indicated if stridor is present during both waking and sleep.
147
What condition may contraindicate the use of CPAP in MSA patients?
Floppy epiglottis may be present in some people with MSA and is a contraindication to CPAP when present.
148
What sleep disorders are people with MSA at increased risk of experiencing?
People with MSA are at increased risk of REM sleep behavior disorder, OSA, central sleep apnea, and sudden death during sleep.
149
What can worsen sleep-related stridor?
Sleep-related stridor can be worsened by the use of sedating medications.
150
In children, what can stridor be a manifestation of?
In children, stridor can be a manifestation of seizure.
151
What is cluster headache?
A headache syndrome marked by very severe, unilateral, periorbital headaches lasting 15 min to 3 h.
152
What are the two characteristic features of cluster headaches?
Their tendency to cluster and their associated autonomic symptoms.
153
How often do patients experience headache clusters?
About once per year, generally lasting 1 to 2 months, with headaches typically occurring daily.
154
What autonomic symptoms are associated with cluster headaches?
Conjunctival injection, tearing, ptosis, eyelid edema, sweating, nasal congestion, and rhinorrhea.
155
What is the association of cluster headaches with REM sleep?
Headache onset frequently occurs during REM sleep, with abnormalities including prolonged REM latency and short REM duration.
156
What is chronic paroxysmal hemicrania?
A headache syndrome similar to cluster headache, with more frequent episodes and shorter episode duration.
157
What are hypnic headaches?
Short-duration, frequent headaches that awaken people from sleep, more often bilateral and not associated with facial autonomic symptoms.
158
How do migraine headaches differ from cluster headaches?
Migraines tend to last longer, are not as likely to cluster, do not have associated facial autonomic features, and are associated with nausea, photophobia, and phonophobia.
159
What is sleep apnea headache?
A headache syndrome defined by the International Classification of Headache Disorders, requiring a headache present on awakening and sleep apnea with an apnea-hypopnea index of >5.
160
What are the additional features for diagnosing sleep apnea headache?
1. Headache onset temporally linked to onset of sleep apnea. 2. Headache worsens or improves with sleep apnea. 3. Headache present at least 15 days/month, resolving within 4 h of awakening.
161
What is a typical quality of sleep apnea headache?
Bilateral headache with a 'pressing' quality that is not associated with nausea, photophobia, or phonophobia.
162
What is the typical age of onset for JME?
The peak age of onset is 12-18 years.
163
What are the characteristics of myoclonus in JME?
Bilateral single or repetitive myoclonic jerks, predominantly in the arms, usually occurring on awakening or in the early morning.
164
What triggers myoclonic jerks in JME?
Sleep deprivation or photic stimulation.
165
What percentage of JME patients eventually develop generalized tonic-clonic seizures?
85%-100% of patients.
166
What are the classic EEG findings in JME?
Rapid, generalized, often irregular spike-waves and polyspike-waves (4-6 hertz).
167
What is the duration of spikes on EEG in JME?
Spikes have a sharp-pointed peak duration of 20 to 70 ms.
168
What distinguishes nocturnal frontal lobe epilepsy (NFLE) from JME?
NFLE seizures are typically associated with paroxysmal dystonia and hypermotor activity, and are generally prolonged.
169
What EEG findings are associated with NFLE?
Focal findings in the frontal regions or motor artifact during the event with no obvious epileptiform discharges.
170
What is a key difference between progressive myoclonic epilepsy and JME?
Progressive myoclonic epilepsy manifests at a younger age and involves a progressive decline in motor skills, balance, and cognitive function.
171
What are sleep starts or hypnic jerks?
Sudden brief contractions of the body or limbs that occur mainly at sleep onset.
172
What sensations accompany hypnic jerks?
A sensation of falling and sometimes auditory or visual hallucinations.
173
What triggers hypnic jerks?
Sleep deprivation and stimulants such as caffeine.
174
How does active depression affect sleep?
Active depression is associated with prolonged sleep latency, decreased REM sleep latency, and slow-wave sleep. It can also blunt the normal circadian rhythmicity of the cardiovascular and endocrine systems.
175
What role does insomnia play in depression?
The development or worsening of insomnia may precede other symptoms of depression, serving as a harbinger of an impending episode.
176
Do sleep derangements improve with treatment of mood disorders?
Most sleep derangements improve with successful treatment of underlying mood disorders, but this is not always the case.
177
What is the impact of psychopharmacotherapy on sleep disorders?
It is vital to consider the impact that psychopharmacotherapy will have on patients with underlying sleep disorders.
178
What is bupropion and how does it affect sleep?
Bupropion is an atypical antidepressant that increases REM-phase sleep but can cause insomnia. It is often used in patients with restless leg syndrome (RLS).
179
How do tricyclic antidepressants (TCAs) affect sleep?
TCAs decrease REM-phase sleep and exacerbate RLS and periodic limb movements of sleep (PLMS). Some are stimulating while others are sedating.
180
What are selective serotonin reuptake inhibitors (SSRIs) and their effects on sleep?
SSRIs decrease total sleep time and are associated with decreased REM-phase sleep, as well as an increase in RLS and PLMS.
181
What are the effects of serotonin and norepinephrine reuptake inhibitors (SNRIs) on sleep?
SNRIs commonly cause insomnia and tend to worsen RLS and PLMS.
182
How does trazodone work and what is its effect on sleep?
Trazodone blocks histamine and alpha-1-adrenergic receptors, causing drowsiness. It is often used for sleep-onset insomnia and does not negatively affect PLMS or RLS.
183
What disorder is suggested by the clinical history in a patient with PWS?
A hypersomnolence disorder.
184
What is excessive daytime sleepiness in PWS thought to be related to?
Hypothalamic dysfunction.
185
What can benefit patients with PWS who experience excessive daytime sleepiness?
A trial of alerting medications.
186
Are patients with PWS at increased risk for obstructive sleep apnea (OSA)?
Yes, especially in the setting of obesity.
187
What did the polysomnographic data indicate for this patient regarding OSA?
The data do not support the diagnosis of OSA.
188
What concerns exist regarding growth hormone in patients with PWS?
It can worsen sleep-disordered breathing (SDB).
189
Is there PSG evidence for SDB in this patient?
No, there is no PSG evidence for SDB.
190
What is the prevalence of PWS?
1 in 10,000-25,000 live births.
191
What causes PWS?
Partial deletion or loss of function of a region on the long arm of paternal chromosome 15 or uniparental disomy.
192
What are some clinical features of PWS in infancy?
Diminished fetal activity, infantile hypotonia, and failure to thrive.
193
What leads to significant weight gain in early childhood for patients with PWS?
Insatiable appetite.
194
What are some other features of PWS?
Short stature, small hands and feet, hypogonadotropic hypogonadism, and intellectual disability.
195
What predisposes patients with PWS to ventilatory problems?
Generalized hypotonia, abnormal arousal and ventilatory responses, scoliosis, and obesity.
196
What can be seen in infancy regarding apnea indices?
Elevated central apnea indices, sometimes associated with sleep-related desaturation.
197
What is common in childhood and adulthood for patients with PWS?
Obstructive sleep-disordered breathing (SDB).
198
What factors contribute to OSA in patients with PWS?
Hypotonia, craniofacial dysmorphism, viscous secretions, adenotonsillar hypertrophy, and obesity.
199
What percentage of adults with PWS may experience excessive daytime sleepiness?
Up to 50%.
200
How is sleep architecture in patients with PWS characterized?
Shorter REM latencies and increased number of REM/NREM cycles.
201
What is the purpose of prescribing growth hormone to patients with PWS?
To improve development, growth, and body composition.
202
Why is PSG often performed before initiating growth hormone therapy?
Due to the commonality of SBD in these patients.
203
What improvements have been reported with growth hormone therapy?
Improvement in resting ventilation and inspiratory drive.
204
What is the community prevalence of PTSD according to epidemiological studies?
Ranges from 1% to 10%.
205
What is a common sleep-related symptom of PTSD?
Nightmares, occurring in up to 70% of affected patients.
206
What is the Veterans Administration/Department of Defense’s guideline regarding benzodiazepines for PTSD?
They caution against the use of benzodiazepines in the management of PTSD.
207
What is the relationship between PTSD and periodic leg movements of sleep (PLMs)?
Patients with PTSD are at increased risk of experiencing PLMs.
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What percentage of veterans with PTSD report difficulty initiating or maintaining sleep?
44%.
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What are the two divisions of the preoptic area?
The preoptic area is divided into the ventrolateral preoptic area (VLPO) and the median preoptic area (MNPO).
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What is the role of VLPO neurons?
VLPO neurons initiate NREM sleep.
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What is the role of MNPO neurons?
MNPO neurons maintain NREM sleep.
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What neurotransmitters are rich in the preoptic area?
The preoptic area contains inhibitory neurotransmitters γ-aminobutyric acid (GABA) and galanin.
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What effect do lesions of the preoptic area have on sleep?
Lesions of the preoptic area produce light and fragmented sleep.
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What type of neurons are found in the basal forebrain?
The basal forebrain contains large groups of cholinergic neurons that promote REM and wakefulness.
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What is the role of GABA-containing neurons in the basal forebrain?
GABA-containing neurons in the BF inhibit the inhibitory cortical interneurons, leading to cortical activation.
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What is the reticular formation?
The reticular formation is a heterogeneous region that spans the medulla, midbrain, and posterior hypothalamus.
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What neurotransmitters are rich in the reticular formation?
The reticular formation includes excitatory neurotransmitters such as acetylcholine, glutamate, norepinephrine, histamine, serotonin, and dopamine.
218
What is the function of the pontine tegmentum?
The pontine tegmentum is involved in the generation of REM sleep.
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What role do acetylcholine-rich neurons in the pontine tegmentum play?
Acetylcholine-rich neurons in the laterodorsal tegmental (LDT) and pedunculopontine tegmental (PPT) nuclei generate cortical activation and atonia of REM sleep.
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How does acetylcholine affect thalamic neurons during REM sleep?
Acetylcholine depolarizes thalamic neurons, leading to the cortical activation necessary for complex dreams.
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What is the effect of acetylcholine on inhibitory neurons in the ventromedial medulla?
Acetylcholine activates inhibitory neurons in the ventromedial medulla that release GABA and glycine, hyperpolarizing brain stem and spinal neurons, leading to atonia.
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Sleep Genes
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What does the clock machinery consist of?
The clock machinery consists of a number of complex transcription/translation feedback loops.
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What do CCGs code for?
CCGs code for CLOCK/BMAL1 protein complex.
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What is the role of the CLOCK/BMAL1 complex?
The CLOCK/BMAL1 complex targets the Cry/Per genes, resulting in transcription of PER and CRY proteins.
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What happens to PER and CRY proteins after transcription?
PER and CRY proteins dimerize in the cytoplasm, re-enter the nucleus, and negatively disrupt the CLOCK-BMAL1 complex.
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What is created as a result of the negative feedback loop?
The negative feedback loop ultimately down-regulates their own transcription.
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Which protein complex starts the new transcriptional cycle within 24 hours?
It is the CLOCK/BMAL1 that starts the new transcriptional cycle within 24 hours.
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What role does Casein kinase 1ε play?
Casein kinase 1ε phosphorylates the PER protein, leading to the degradation of the repressor complex CRY/PER and slows down transcription.
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What allows CLOCK/BMAL1 to start the new transcriptional cycle?
The activation of specialized genes called F-Box allows CLOCK/BMAL1 to start the new transcriptional cycle.
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What is noted about CCG panels in different tissues?
There is a significant difference in CCG panels between peripheral tissues and the suprachiasmatic nucleus.
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What regulates circadian rhythms?
CLOCK/BMAL1 is the positive arm of the feedback loop regulating circadian rhythms.
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What do CLOCK/BMAL1 proteins bind to?
CLOCK/BMAL1 proteins bind to specific DNA elements in the regulatory regions of the CCG, including those coding for CRY/PER.
