insomnia Flashcards
Which type of behavioral therapy for childhood insomnia is analogous to stimulus control?
Graduated extinction
Which of the following is true regarding the use of actigraphy to diagnose insomnia?
Compared with sleep logs, actigraphy provides similar information about total sleep time and sleep latency in response to treatment
In Genome Wide Association studies of insomnia symptoms, which gene, previously implicated in another sleep disorder, was associated with insomnia?
MEIS1, Restless Legs Syndrome
According to the AASM Clinical Practice Guideline for Pharmacologic Treatment of Insomnia, which of the following is true about the medications recommended for pharmacologic treatment of sleep maintenance insomnia?
None of the treatments decreased WASO more than 30 minutes
Among adults with insomnia symptoms or DSM-IV insomnia syndrome at baseline, what percent will have insomnia at least 1 year over the next 3 years?
74%
Compare zolpidem to doxepin
Zolpidem was associated with higher fall risk and more difficulty with arousal
What is the incidence of transient insomnia at one year
40%
What is the Incidence of different types of insomnia
Sleep onset insomnia 23%
Sleep maintenance insomnia 32%
Mixed insomnia 17%
Combined insomnia 29%
What is adjustment sleep disorder
Associated with a specific stress or
What is Psychophysiologic insomnia
Heightened arousal and learned sleep preventing associations
What is Paradoxical insomnia
Subjective report of severe sleepiness not congruent with the absence of sleep or minor degree of daytime impairment
What is Idiopathic insomnia
Onset in childhood or infancy
What is Inadequate sleep hygiene
Associated with activities that are inconsistent with optimal sleep
What is Behavioral insomnia of childhood
Result of inappropriate sleep associations or inadequate limit setting
What is the prevalence of chronic insomnia
10
Chronic Insomnia Disorder
A. The patient reports, or the patient’s parent or caregiver observes, one or more of the following:1
1. Difficulty initiating sleep. 2. Difficulty maintaining sleep. 3. Waking up earlier than desired. 4. Resistance to going to bed on appropriate schedule. 5. Difficulty sleeping without parent or caregiver intervention.
Chronic Insomnia Disorder
The patient reports, or the patient’s parent or caregiver observes, one or more of the following related to the nighttime sleep difficulty:
1. Fatigue/malaise. 2. Attention, concentration, or memory impairment. 3. Impaired social, family, occupational, or academic performance. 4. Mood disturbance/irritability. 5. Daytime sleepiness. 6. Behavioral problems (e.g., hyperactivity, impulsivity, aggression). 7. Reduced motivation/energy/initiative. 8. Proneness for errors/accidents. 9. Concerns about or dissatisfaction with sleep.
Comorbid insomnia and psychiatric disorders
Insomnia is correlated with the likelihood of having at least 1 psychiatric diagnosis with an odds ratio of 5.0 for severe insomnia
In a large European study, 18% of the population reported insomnia of 6 months duration or longer, and of those 48% had a current psychiatric disorder by DSM-IV
Medications for psychiatric disorders can affect sleep
Medications for sleep disorders can affect psychiatric symptoms
Prevalence of Insomnia in OSA ?
A high prevalence (39%-58%) ofinsomniasymptoms have been reported in patients withOSA
Do insomniacs have apnea hypopnea index greater than 5?
Between 29% and 67% of patients withinsomniahave an apnea-hypopnea index of greater than 5
Does CBTi work for patients with OSA?
Combination therapy, of CBTI and OSA treatment, resulted in greater improvements ininsomniathan did either CBTI orOSAtreatment alon
What is the effect of exercise on sleep?
Acute exercise has small self reported benefits on total sleep time, sleep onset latency, sleep efficiency and moderate benefits for wake after sleep onset.
Regular exercise has small self reported benefits on total sleep time, sleep efficiency, sleep latency, and moderate benefits on sleep quality
What are benefits of cognitive therapy ?
Address thoughts and beliefs that interfere with sleep.
What are benefits of relaxation training?
Reduce arousal & decrease anxiety
How does sleep restriction work?
Restrict time in bed to improve sleep depth & consolidation
Determine average time asleep based on baseline sleep diary
Set time in bed = time asleep
Consistent wake-up time
No daytime naps
If time asleep > 85% of time in bed then increase time in bed (15-20 minutes)
If time asleep < 80% of time in bed then decrease time in bed (15-20 minutes)
Time in bed increases continue as long as sleep efficiency > 85% until patient reports optimal daytime functioning
What is stimulus control?
Strengthen bed & bedroom as sleep stimulus
Use bed for sleep and sex only
Go to bed only when sleepy
Get out of bed when unable to sleep after approximately 15-20 minutes
Wake up at a consistent time, including weekends
Avoid daytime naps
What is sleep hygiene?
Promote habits that help sleep; provide rationale for subsequent instructions.
Regularize sleep / wake schedule Avoid stimulants and stimulating behavior Establish relaxing bedtime routine Provide conducive sleep environment Limit daytime naps Reduce or eliminate alcohol and caffeine Obtain regular exercise Avoid clock watching
What are most commonly used sleeping pills?
medications commonly used for insomnia (MCUFI)
3% on MUCFI and 55% of MCUFI users take at least one other sedating medication and 10% take ≥ 3
High rates of MCUFI among elderly and individuals seeing mental health provider
Most commonly prescribed Trazodone & Zolpidem
Neurotransmitters promoting arousal
Acetylcholine Dopamine Glutamate Histamine Norepinephrine Orexin 1 and 2 Serotonin
Neurotransmitters promoting sleep
Adenosine GABA Galanin Glycine Melatonin
What are the kinetics of Zaleplon®
onset 10-20 min half-life 1.0 dose 5-20 mg
What are the kinetics of Zolpidem®
onset 10-20 min half-life 1.5-2.4 dose 5-10 mg
What are the kinetics of Zolpidem CR®
onset 10-30 min half-life 3-4.5 dose 6.25-12.5 mg
What are the kinetics of Eszopiclone®
onset 10 min half-life 5-7 dose 1-3 mg
What are the kinetics of Triazolam®
onset 10-20 min half-life 1.5-5 dose 0.125-0.25 mg
What are the kinetics of Temazepam®
onset 45-60 min half-life 1 8-20 dose 7.5-30 mg
What are the kinetics of Flurazepam®
onset 15-30 min half-life 36-120 dose 15-30 mg
What are the kinetics of Quazepam®
onset 15-30 min half-life 15-120 dose 7.5-15 mg
What are Benzodiazepine Receptor Agonists: Effects on Sleep
Sleep continuity ↓ Sleep latency ↓Awakenings ↑ Sleep Duration ↓ Slow Wave Sleep (BZs only) ↓ REM (BZs only) ↑ Duration and number of sleep spindles ↓Periodic limb movements and associated arousals
What are BZA side effects
Daytime Sedation Cognitive/motor impairment Anterograde amnesia Rebound insomnia upon discontinuation Parasomnia Tolerance/dependence/abuse/withdrawal (DEA schedule IV)
What zolpidem effects
Associated with Longer total sleep time Fewer awakenings after sleep onset Shorter sleep latency Greater ease of falling asleep Better quality of sleep Increased sleep efficiency
What are features of melatonin
1.3% or 3.1 million US adults use melatonin based on surveys from 2002-2012 per the National Health Statistics Reports, 2015
Melatonin use among adults in the US more than doubled between 2007 and 2012.
Ramelteon, a melatonin receptor agonist, does not affect AHI or oxygenation in mild to moderate OSA
Describe Suvorexant
Suvorexant is a dual orexin receptor antagonist, the first in this new class of medications
Half life 12 hours
Recommended dosing: 10mg within 30 minutes before going to bed, in patients who plan to sleep continuously for at least 7 hours, with a maximum dose of 20mg
Dose reduction should be considered in obese females, or patients taking moderate CYP3A4 inhibitors; excreted in feces and renally
What is the effect of SSRI on sleep
Decrease REM and sometimes SWS
What is the effect of mirtazepine on sleep
Increase sleep continuity
What is the effect of trazodone on sleep
Increase sleep continuity
Describe pharmacotherapy antihistamines on sleep
Mechanism of action
H1 receptor antagonism
Variable antagonism of cholinergic, serotonergic, adrenergic receptors
Adverse effects Sedation, grogginess Dry mouth Psychomotor impairment Delirium
What the effects of hormone replacement therapy on sleep.
Studies have shown that women on HRT seem to fall asleep faster, have longer periods of REM sleep, have fewer arousals, and sleep longer than those not on HRT. Taking HRT at bedtime seems to be the most helpful timing of drug.
What are side effects of high doses, valerian
blurred vision, excitability and cardiac arrhythmias.
What are side effects of kava
The FDA has also warned that kava may be linked to serious liver damage and in addition should not be used by persons with cardiovascular disease.
What are the sleep architecture effects of Clomipramine
Clomipramine, a tricyclic antidepressant, is one of the most potent REM suppressing drugs available. Other tricyclic drugs and SSRIs tend to cause a more modest suppression of REM sleep.
What are the sleep architecture effects of Trazodone and nefazodone
Trazodone and nefazodone have fewer effects on REM, and some reports have even shown an increase in REM sleep. In general, antidepressants have few effects on slow wave sleep. However, tertiary tricyclic antidepressants and trazodone have been found to increase slow wave sleep in some studies.
Can benzodiazepines help PAP Therapy
benzodiazepines may be of benefit in promoting sleep and improving tolerance of PAP. Non-benzodiazepine benzodiazepine receptor agonists such as zolpidem and eszopiclone do not affect obstructive sleep apnea AHI or SpO2. Multiple studies show improved adherence to PAP therapy when the patient is concurrently initiated on a Non-benzodiazepine benzodiazepine receptor agonists.
What are the side effects of zolpidem
The most common side effects of zolpidem may include nausea, dizziness, malaise, nightmares, agitation, headaches.Do not see rebound insomnia between nights of treatment and drug-free nights. Zolpidem as-needed administration may allow patients to adapt treatment to their needs and to the evolution of their insomnia.
Where the effect sizes of benzodiazepines for sleep.
The effect of benzodiazepine receptor agonists versus placebo was measured as the effect size d, which is a standardized measure of the difference between active treatment and placebo. By convention, effect sizes below 0.5 are considered small, between 0.5 and 0.8 moderate, and above 0.8 large. On measures of self-reported sleep latency, total sleep time (TST), number of awakenings, and sleep quality, benzodiazepine receptor showed a consistently superior effects to placebo. The effect sizes were moderately large, demonstrating that these drugs are indeed efficacious for short-term treatment.
Describe the effects of sleep restriction
Sleep Restriction Therapy is designed to consolidate sleep by increasing sleep drive. The technique involves an initial reduction in the time spent in bed followed by a gradual extension of time in bed, The patient is initially prescribed a time-in-bed period that is roughly equal in length to the total amount of sleep reported on baseline sleep diaries. The actual placement of the sleep period should be determined based on the patient’s circadian rhythm preference and specific life constraints. The minimum time in bed recommended is 5 hours nightly. When sleep efficiency is at least 85% on average for approximately 1 week, the time in bed is increased by 15-20 minutes if the patient reports adverse daytime consequences. Increases in time spent in bed continue in 15-20 minute increments per week, as long as the sleep efficiency remains above 85% When sleep efficiency drops below 80%, time-in-bed is decreased by 15-20 minutes until sleep efficiency increases above 85%.
Sleep Heart study and insomnia
There is a 29% higher risk of cardiovascular disease in the insomnia group
Insomnia or poor sleep was not associated with all cause mortality
What neuroanatomic findings occur in insomnia patient’s
Insula is a critical region for sleep maintenance
Prefrontal cortex and default mode neck or may play crucial role and cognition dysfunction
Increased Activity between right auditory language comprehension Center in executive control network leads to inability to disengage from external auditory stimulation and leads to hyperarousal
Actigraphy versus sleep diaries in insomnia evaluation
Compared to sleep diaries actigraphy
Estimated a mean of 38 minutes more sleep in intervention studies and 35 minutes in non-intervention studies
How does actigraphy compared to polysomnogram
Compared to PSG it estimates 10 extra minutes of sleep
How does actigraphy compared to Diary in sleep late
Compared to PSG it estimates 8 less minutes of sleep Latency
Compare agents regarding sleep latency
Lunesta and 14 minute decrease in sleep latency with a moderate to large effect.
Ramelteon had a 9 minute decrease in sleep latency with no improvement in sleep quality
Temazepam had a 37 minute reduction in sleep latency with a small affect and sleep quality. Triazolam had a 9 minute reduction in sleep latency with a moderate improvement in sleep quality zaleplon and a 10 minute decrease in sleep latency with no improvement in sleep quality resulted in had a 5-12 minute decrease in sleep latency with a moderate sleep quality
Compare agents regarding sleep maintenance
In sleep maintenance
Doxepin 26-32 minutes small to moderate
Lunesta 2857 minutes moderate to large
Restoril 99 minutes small
suvorexant 10 minutes
Zolpidem 29 minutes moderate
Compare agents altogether
Sleep onset is ramelteon triazolam and zaleplon
Sleep maintenance is doxepin and suverexant
Both is Lunesta zolpidem and temazepam
What percentage of people feel medication helps insomnia
67% of people using long-term hypnotic medications to help them sleep rated their sleep quality as improved and only 14% reported little or no improvement
What are risks of insomnia
Insomnia patients have substantially increased risk of future mood and psychiatric disorders higher health care use and costs elevated risk of falling reduced quality of life increased absenteeism and cognitive impairments
How long do insomniacs use medication
70% of insomniacs use for two weeks or less.
What are the PharmaKinetics a melatonin
melatonin has a maximum concentration of about .5 hours and elimination half-life of one hour. It is effective for sleep onset. It may be associated with reversible inhibition of spermatogenesis and ovulation
What are Pharmacokinetics of ramelteon
Ramelteon is a half-life of 1 to 2.5 hours. Therapeutic dose of 8 mg is given 30 minutes before bedtime.
When is doxepin effective
Doxepin is more effective in the last third of the night.
What are the PharmaKinetics of trazodone
Trazodone t max of 1 to 2 hours and a half-life of 7 to 15 hours.
What are the effects of gabapentin
Gabapentin exerts its fact through binding to the alpha-2 Delta subunit of the N type voltage gated calcium channel. T max is 3.5 hours and half-life is 5 to 9 hours. Used in people with restless leg syndrome alcohol dependence and seizure disorder
What is the role of sodium oxybate
Sodium oxybate has a Tmax of .5 to .8 and a half life of .3 - 1.2 hours. It is dose to bedtime and in the middle of the night is dosed in the range of 2.5 to 4.5 g. Side effects include Parasomnias celebration nausea and vomiting and amnesia. It should not be used in people with respiratory depression including those with sleep disordered breathing and COPD.
Exceptions to three month rule for diagnosis of insomnia
– Patients with recurrent episodes lasting several weeks at a time over several years, yet not meeting the 3-month duration criterion for any single episode may be diagnosed as chronic
– Patients sleeping well with the use of a hypnotic
medication who would meet the criteria without the
medication - especially when voicing concerns about their inability to sleep without sleep medication
Performance issues that must be present to diagnose insomnia
- Fatigue/malaise
- Attention, concentration, or memory impairment
- Impaired social, family, occupational, or academic performance
- Mood disturbance, irritability
- Daytime sleepiness
- Behavioral problems (e.g., hyperactivity, impulsivity, aggression)
- Reduced motivation/energy/initiative
- Proneness for errors/accidents
- Concerns about or dissatisfaction with sleep
What are Insomnia Treatment Modalities
• Sleep hygiene recommendations • Psychotherapeutic techniques • Behavioral strategies • Cognitive behavioral therapy for insomnia (CBT-I) • Light/dark exposure • Schedule manipulations • Pharmacotherapeutic: – Substances – Medications
What are the Components of CBT-I
• Cognitive therapy strategies • Sleep restriction therapy • Stimulus control therapy • Relaxation therapy • Sleep hygiene education and rules • Paradoxical intention • Biofeedback • Multicomponent therapy without cognitive therapy
What cognitive distortions does cognitive psychotherapy attempt to correct
• Chronic insomnia patients often:
– Assume daytime problems result from poor sleep
– View transient sleep problems as chronic
– Have unrealistic expectations about their sleep need
– Exhibit cognitive errors: overgeneralization,
rumination, and magnification
– Have high anxiety associated with attempts to fall
asleep
What are Sleep Restriction Therapy guidelines
• Initial prescribed time in bed (TIB) determined by
average sleep from 2-week sleep log
– Awaken by alarm same time 7 days a week
– Bedtime delayed for restricted schedule
– No napping
– (Do not limit TIB to less than 5 hours)
• TIB bedtime adjustments are made each week
– If sleep efficiency is 90% or greater, bedtime is adjusted 15
to 30 minutes earlier
– If sleep efficiency is 85% or less, bedtime is adjusted 15
minutes later
• Treatment course typically is 6 to 8 weeks
What is Stimulus Control Therapy
• Developed by Richard Bootzin (1970s)
• Addresses the reinforced association between
the bed, bedroom, and attempts to fall asleep
in relation to excessive arousal, prolonged
wakefulness, and frustration
• Essentially, deconditions while some sleep
deprivation promotes a reassociation of going
to bed with successful sleep onset
Trazodone
Biphasic T½ – 3 to 6 hours – 5 to 9 hours Onset 30 – 120 minutes Receptor effects – 5-HT2A,2B receptor antagonist – 5-HT1A partial agonist – α1 -receptor antagonist – α2 -receptor antagonist – Histamine H1 antagonist – Serotonin reuptake inhibition Side effects – Dizziness– Sedation– Hypotension– Headache– Sweating– Arrhythmias– Priapism– Serotonin syndrome Active metabolite: mCPP
What are GABA A Alpha Subunit Subtypes
α Subtype % of CNS GABA A receptors Known Action Mediated α1 % of receptors 60 Sedation, amnesia, ataxia (!)
α2 15 - % of receptors 20 Anxiolytic, myorelaxation α3 10 - 15 Myorelaxation (high doses), ataxia
α4 % of receptors < 5 Insensitive to BZRAs
α5 % of receptors < 5 Partial myorelaxation, ataxia
α6 % of receptors < 5 Insensitive to BZRAs
Benzodiazepines Immediate Release
Estazolam ProSom Dose 1, 2 half-life 10 to 24
Flurazepam Dalmane Dose 15, 30 half-life 2.3 (active metabolite: 48 - 160)
Quazepam Doral Dose 7.5, half-life 15 39 (active metabolite 73)
Temazepam Restoril Dose 7.5, 15, 22.5, 30 half-life 3.5 to 18.4
Triazolam Halcion Dose 0.125, 0.25 half-life 1.5 to 5.5
Nonbenzodiazepines Immediate Release
Eszopiclone Lunesta dose 1, 2, 3 half-life ~6 (~9 in elderly)
Zaleplon Sonata dose 5, 10 half-life 1
Zolpidem Ambien dose 5, 10 half-life ~2.5
Nonbenzodiazepines Alternate Delivery
Zolpidem oral spray Zolpimist dose 5, 10 2.7 – half-life 3.0
Zolpidem sublingual Edluar dose 5, 10 half-life ~2.5
Zolpidem sublingual Intermezzo dose 1.75, 3.5 half-life ~2.5
Nonbenzodiazepines Extended Release
Zolpidem ER Ambien dose CR 6.25, half-life 12.5 2.8 in males (longer in females)
What are Discontinuation Effects of sleeping pills
• Rebound insomnia: Sleep is worsened relative
to baseline for 1 to 2 nights after
discontinuation. More likely with higher doses
and short/intermediate half-life hypnotics
• Recrudescence: Return of original insomnia
symptoms
• Withdrawal: New cluster of symptoms not
present prior to treatment (e.g., anxiety,
seizures)
What was the 2014 Update Drug Safety Communication regarding Eszopiclone
FDA Recommends lower initial dose for men and women to be 1 mg at bedtime
What are BZRA Hypnotics Possible Adverse Effects
- Residual effects
- Dizziness
- Headache
- Somnolence
- Blurred vision
- Nausea/diarrhea
- Fatigue
- Ataxia
- Anterograde amnesia
- Somnambulism/complex sleep behaviors
What are efects of Ramelteon
• FDA approval: Indicated for the treatment of insomnia characterized by difficulty with sleep onset • No limitation on duration of use • Non-sedating • Single dose: 8 mg (Flat dose-response relationship) • Take about 30 minutes prior to bedtime • Avoid hazardous activities after dose • Elimination half-life 1 – 2.6 hours Adverse events – Somnolence (5%) – Dizziness (5%) – Fatigue (4%) Avoid with – Hepatic impairment (moderate to severe) – Fluvoxamine (Luvox) coadministration
What are Doxepin adverse effects
Most common adverse events – Somnolence/sedation – Nausea – Upper respiratory tract infection Elimination half-life: 15.3 hours
How do you use Suvorexant
USE:
– 10 mg taken only once
– Within 30 minutes of going to bed
– At least 7 hours remaining before the planned
time of awakening
– Dose may be increased to a maximum of 20 mg
– 5 mg is recommended for people talking a
moderate CYP3A4 inhibitor
– Time to effect may be delayed with food
What is pathogenesis of primary insomnia which is a state of physiologic hyperarousal
Meeting sleep latencies on an SLT or higher are comparable to those of controls
Increased 24-hour metabolic rate
Increased global cerebral glucose metabolism awake and asleep on PET
Increased beta and decreased data delta EEG activity during sleep
Increased ACTH and cortisol secretion
What are Elimination half-lives of hypnotic agents
• Less than 1 hour: – Ramelteon – Zaleplon • 2 to 6 hours: – Eszopiclone Triazolam – Zolpidem • 6 to 24 hours: – Doxepin (low-dose) – Estazolam – Temazepam – Suvorexant Greater than 40 hours: – Flurazepam – Quazepam
There is insufficient evidence for the effectiveness in insomnia of
Cognitive therapy alone
Sleep hygiene education alone
Imagery training alone
There is sufficient evidence for effectiveness of
Stimulus control therapy Relaxation training Sleep restriction Multicomponent therapy without cognitive therapy Paradoxical intention Biofeedback
What characterizes non-benzodiazepine benzodiazepine receptor agonist
Similar hypnotic action to benzodiazepines
No muscle relaxant anticonvulsant or anxiolytic properties
Not likely to cause rebound insomnia withdrawal symptoms or tolerance or to alter sleep architecture
What are the cardiovascular effects of sleep duration
Long and short sleep duration cause all cause mortality hypertension obesity and diabetes
What condition is associated with H Per2 gene
Advanced phase sleep disorder
What effect does evening light have on advanced sleep disorder.
Evening light has a week therapeutic effect on advanced sleep disorder. 4000 lx for 2 hours Duration 12 days Increasing total sleep time Main phase delay is 2.4 hours
What is epidemiology of narcolepsy
Contrary to widely held views, narcolepsy is not a rare disorder. Well designed studies have shown that the prevalence of narcolepsy with cataplexy in western European countries and North America approaches 0.05% (range 0.02% - 0.06%), or one case for every 2,000 people.1 This figure is not very different from that reported for multiple sclerosis (range 0.06% - 0.14%), another common neurological disorder.2 Some studies have shown that narcolepsy may be more frequent in Japan and rare in Israel.
What are essential and associated symptoms of narcolepsy
Essential
Excessive daytime sleepiness (EDS)
Cataplexy
Associated
Hypnagogic hallucinations
Sleep paralysis
Disturbed nocturnal sleep
Excessive daytime sleepiness
Sleep attacks on a background of chronic sleepiness or fatigue Frequent napping, usually refreshing Memory lapses and automatic behaviors Impaired attention / concentration Decreased work performance Increased drowsy driving crashes Visual disturbances
What is incidence of difficulty falling asleep or staying asleep
Insomnia is a common complaint in the population in general. Studies suggest that up to 30-40% of the population complain of difficulty falling or staying asleep, or non-restful sleep.
What is the prevalence of insomnia
Insomnia that is also associated with daytime impairment or significant distress constitutes the general definition of insomnia as a disorder and is less common than the complaint of sleep disturbance alone (8-19%).
What is the differtence in prevalence of insomnia with men compared to women
Insomnia is more likely to be reported by A meta-analysis found that women are almost 50% as likely to develop insomnia compared with men (relative risk 1.41).
The difference in insomnia prevalence between men and women increases with age, and reaches greatest significance in the post-menopausal period.
Risk factors for insomnia
Previous history of insomnia
Increasing age
Female sex
Psychiatric symptoms and disorders
Medical symptoms and disorders
Stress
Lower socioeconomic status
Fewer years of education
What factors disrupt sleep in pregnancy:
Nocturia
Gastroesophageal reflux
Hormonal changes such as oxytocin release in late pregnancy
Fetal movements & contractions
Musculoskeletal pain
Sleep disorders which develop during pregnancy (OSA and RLS)
What factors that impact sleep quality in menopause
Reproductive hormone levels
Mood symptoms
Vasomotor symptoms
What are risks of insomnia in women
Impact on pregnancy and post-partum course
Association with pre-term birth
Association with longer labor and cesarean deliveries
Higher risk of incident and recurrent post-partum depression
Deficits in post-partum neurobehavioral performance
Increased pain in fibromyalgia
What are some Class C (potential benefit outweighs risk) drugs to avoid in pregnancy
zaleplon, eszopliclone, zolpidem, ramelteon, gabapentin, doxepin and trazodone
What is graduated extinction
Graduated extinction consisted of the parent putting the child to bed and ignoring the tantrum activity for increasingly longer amounts of time throughout the treatment.
