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40 y/o with insomnia after death of his brother. ANSS without OSA or PLMD. Dx?: Adjustment sleep disorder.
Effect of benzos on sleep stages? Non-benzo hypnotics?: Benzos increase stage II. Decrease REM, SWS. Non BZ agents do not decrease SWS or REM.
Morning anxiety in patient using triazolam?: Rebound anxiety can be seen with shorter acting agents.
Nefazodone (Serzon) mechanism?: Blocks 5HT2 and serotonin reuptake.
Mirtazapine (Remeron) mechanism?: Alpha-2 blocker (increases NE and serotonin), 5HT2, 5HT3 blocker.
Hypnotic agent for mid-cycle awakenings?: Sonata - shortest half-life.
30 y/o woman with several year hx of sleep init/maintenance insomnia. Sleeps okay when traveling. Has normal ANSS. Why?: Psychophysiological insomnia. If less than 6 monhs, this is adjustment sleep disorder. Normal ANSS cold also indicate sleep state misperception.
Reverse first night effect?: Good night sleep in the lab. Suggests psychophysiological insomnia or problem with home sleep environment.
Cyclic activity in chin EMG suggests this dx.: Bruxism
Prevalence in kids and adults. Risk factors?: 20-88% in kids (before adult teeth come in). Approx 3% of adults over 60. Smokers may have more bruxism.
Medications causing bruxism? Other possible causes?: Levodopa, SSRIs. Stress, tooth malocclusion.
Associated sx?: Headache, TMJ pain,
Bruxism most common in which stages?: II, REM (tonic)
Treatment for bruxism?: Nothing proven in clinical trial. Mouthguard may help. Many meds tried: levodopa, benzos, muscle relaxants, relaxation therapy, biofeedback, hypnosis.
Typical EMG pattern in bruxism?: "Checkerboard" pattern.
Percent of seizure occuring only during sleep?: 10-40%
Order of seizure threshold from low to high in wakefulness, REM, NREM sleep?: REM, wake, NREM. (Highest chance of a seziure in NREM sleep.)
EEG pattern for seizures? Usual direction of initial deflection?: Spike and wave. Negative (up).
Correct way to amplify a nasal pressure signal on PSG?: DC signal or AC with long time constant or very small low filter setting (<=0.01).
Three factors influencing degree of O2 desat in OSA patients.: Waking supine PaO2, amount of sleep spent in apnea, and ERV.
Causes of a false negative sleep study?: Abstinence from usual alcohol or sedative use. Mild OSA can show more night to night variability. Lack of REM or supine sleep.
Minimum amount of sleep required for diagnostic portion of split night study.: Two hours.
Minimum AHI for split study.: AHI > 20 with desats; > 40 if no associated findings.
Shape of expiratory flow curve in a central apnea?: Round.
No change in body position with fluctuating level of recorded leak - probably source of leak?: Mouth
"Symptomatic" according to Medicare guidelines for CPAP treatment.: EDS, HTN, ischemic heart dz, stroke, insomnia, mood disorder.
Does sham nasal CPAP improve subjective daytime sleepiness?: Yes. Placebo effect documented in 1999 Lancet article.
Medicare definition of hypopnea.: >=30% reduction in airflow with 4% desat. Does not include arousals without desats.
Do split night studied over- or underestimate OSA severity.: Usually underestimate. Don't record as much supine/REM sleep.
Possibly useful types of positive airway pressure for patient who has trouble tolerating high pressures needed in specific position or sleep stage.: BiPAP or Auto-CPAP
Usual method of titrating BiPAP.: Keep IPAP=EPAP and increase both until apneas resolve. Then increase IPAP until hypopnea and snoring resolves. Or, start at 6/4 and sequentially increase IPAP then EPAP to desired effect.
BiPAP helpful for mouth leak?: Yes. Not studied, but sometimes you can get away with less pressure.
If there are persistent apnea, do you adjust IPAP or EPAP? And for persistent hypopneas?: Increase EPAP for apneas, IPAP for hypopneas (and snore).
Potential cause of hypoxia during REM immediately after adequate CPAP titration?: Can have more REM d/t rebound, with hypoventilation during REM.
How to treat hypoxia/hypercapnia in obese pts. with OSA? Is it permanent?: Consider bilevel pressure or volume cycled mode. Ventilation usually improves after few weeks on CPAP.
Patients that do best with UPPP?: Those with upper airway narrowing limited to retropalatal area.
Failed UPPP cases: most common site of failure?: Retropalatal area.
Less common but severe cause of failure post UPPP?: Nasopharyngeal inlet stenosis.
Post-op UPPP complications?: Pain. Velopharyngeal incompetence (snarfing). Change in voice. Globus. Worsened OSA.
Poor candidates for oral appliance?: Pre-existing TMJ. Not in book but according to Dr. Rosen: very large neck.
Two major types of oral appliance?: Tongue retaining device and mandibular advancing device.
Criteria for safety clearnace using MWT?: None have been established.
"Normal" MWT results?: Stay awake more than 19 minutes on a 40 minute test or 11 minutes on a 20 minute test.
Things that worsen simple snoring?: Anything that narrows upper airway, increases nasal resistance, decreases upper airway muscle tone: sedatives, supine position, nasal congestion.
Prevalence of habitual snoring over age 40?: Some studies suggest 60% men 40% women.
Intensity of snoring and stage of sleep?: Loudest in SWS, quietest in REM.
Do thermistors detect snoring?: No. But nasal pressure xducer or pneumotachograph can.
EMG chin pattern sometimes seen with snoring?: Increase in chin EMG activity at inspiration.
Stage of sleep with loudest snoring?: Stage IV
Can you have UARS without excess daytime somnolence?: No
Why would someone with Prader-Willi have prolonged elevation of transcutaneous CO2 and hypoxia without frank obstructive events?: Markedly blunted hypoxic ventilatory response, especially in peripheral chemoreceptors. The hypercapneic response can be blunted, mainly in the obese.
Chromosome usually affected in Prader Willi?: 15
Are hypnotics safe in patients with COPD?: Minimal effect on breathing if stable COPD (not overlap syndrome) with normal daytime CO2.
Does nocturnal O2 cause CO2 retention?: Should not as long as there is no sleep apnea present.
DDx of nocturnal awakenings in patients with asthma?: Diurnal reduction in airflow vs. OSA. FEV1 hits nadir at 4am. Treating OSA can also help control the asthma.
Timing of arousal in Cheyne Stokes vs. idiopathic central apnea?: C-S apnea - arousal usually at peak ventilatory effort. Idiopathic - usually at apnea termination.
Tx of idiopathic central sleep apnea?: Debatable. CPAP, oxygen, triazolam, inhaled CO2, acetazolamide all listed.
Two top causes of Cheyne Stokes breathing?: CHF and stroke
Prevalence of C-S apneas in severe CHF?: "As high as" 40-50%
Difference in daytime pCO2 in CHF patients with or without Cheyne Stokes?: Lower pCO2 in Cheyne Stokes patients.
Difference in hypercapneic ventilatory drive in CHF patients with or without Cheyne Stokes breathing (CSB)?: Higher drive in CSB patients.
Difference in LV filling pressure in CHF patients with or without Cheyne Stokes?: Higher LV filling pressure in CSB.
Effect of higher filling pressures on ventilation?: Can stimulate lung receptors, lead to increased ventilation.
Why does CPAP help CSB? Three reasons (in theory).: Improve LV function, increase O2 stores (less desat), and slightly increase pCO2.
How does adaptive servo ventilation work?: During hypoventilation, the IPAP/EPAP difference widens. Narrows during increased ventilation. Usually maintains minimum of EPAP 5. Can have back up rate.
Usual PSG finding in congenital central hypoventilation?: Reduced tidalvolume and respiratory rate. Central apneas not common.
Why would ventilation be worse in NREM sleep for CCHS patients?: Metabolic control of ventilation occurs during NREM; durin REM, there is less related to hypoxic/hypercapenic input.
Two disease associationg seen with CCHS?: Hirschsprung dz and neuroblastomas.
Are peripheral chemo-receptors functional in CCHS?: Yes. (AK - One study showed passive pedaling of legs during sleep reduced pCO2 in these patients.)
Are leg movements associated with apnea termination counted towards the PLMI?: No.
If there is a periodic movement in the left leg >5 seconds after onset of a periodic movement in the right leg, are the events counted as one or two?: Two. More than 5 secs apart and they're separate events.
Difference between a leg movement and a periodic leg movement?: PLM has to be part of 4 repetitive movements, not associated with apnea termination or after an arousal.
Criteria for counting a leg movement?: Lasts 0.5 to 5 secs and is at least 25% amplitude seen in the biocal. These criteria can vary.
ICSD categorization of PLMs into mild, mod, severe?: 5-24 mild; 25-49 moderate; > 50 severe. PLMA index > 25 is severe. Not based on any data.
Frequency of augmentation when RLS treated with carbidopa? If PLMS tx'd with crabidopa?: Up to 80% in RLS and 30% in PLMS.
First step if you see augmentation with Mirapex?: Treat earlier in the evening.
Side effects seen in Mirapex?: Nausea, hypotension, somnolence, headache, and rare lower extremity edema.
If you get nausea or augmentation with mirapex, what advice do you give?: Try splitting dose - half at 6p half at 8p.
Requip side effects?: Nausea, somnolence, postural hypotension.
Mechanism of clearnace in requip? In Mirapex?: Requip = hepatic; mirapex = renal.
% of narcolepsy patients with cataplexy: 70%
Concordance in twins?: 25-30%
% of narcolepsy cases starting over age 50?: 5%
Percent of narcoleptics with the tetrad (cataplexy, hypnagogic hallucination, sleep paralysis, sleep attacks)?: 10-15%
Is cataplectic weakness ever asymmetric?: No.
Abnormally low REM latency? Percent of narcoleptics wit this PSG finding?: Less than 20 mins. 40-50%.
Probablility of a positive MSLT (two REM naps and mean sleep latency < 5 mins) in a narcoleptic?: 70-80%
Generic name of Dexedrine? Dexosyn? Ritalin?: Dextroamphetamine. Methamphetamine. Methylphenidate.
Major toxicity of pemoline?: Liver
Nonpharmacologiscal methods to treat narcolepsy?: Sleep hygiene, scheduled naps, adequate sleep time.
Most common side effect of Provigil? How to avoid it?: Headache. Can start at 100mg for a few days before increasing dose.
Important warning for women taking Provigil?: Reduced efficacy of birth control meds.
Alternative therapy to stimulants in narcoleptics?: Selegiline - alerting and anticataplectic properties. Irreversible MAO type B inhibitor. Has non-selective MAO inhibition abotve 20mg dose. Need low tyramine diet.
Does negative HLA DQB1*602 rule out narcolepsy? How many narcoleptics are negative?: No. 1-5%.
Approach to persistent sleepiness in OSA?: Check compliance, rule out concurrent sleep disorders. MSLT with CPAP can show narcolepsy in right clinical scenario.
Other haplotypes associated with narcolepsy?: HLA-DR2. HLA-DR15 (negative in 40% of African Americans).
Familial cases of idiopathic hypersomnia associated with which HLA?: HLA-Cw2
Associated symptoms in familial IH?: Autonomic dysfunction - hypotension, Raynaud's, syncope.
Hypersomnia after head injury?: Posttraumatic hypersomnia develops 6-18 months after accident.
Clue to depression on PSG?: REM latency less than 60 mins.
Things to rule out prior to making diagnosis of IH?: Depression, hydrocephalus, meds/abuse, insufficient sleep, UARS or OSA, PLMS.
MSLT findings in IH?: Latency < 10 mins, less than two REM naps.
Stage of sleep associated with bruxism?: Stage II
Does sleepwalking require a psych eval?: No. Usually not associated with psychopathology. Book says "at least" 50% of adults who sleepwalk don't have psychpathology. Sounds like a lot of psychopathology to me.
When does sleepwalking occur?: Classically in SWS (first third of night), especially in kids. Can occur in stage II, so it may be seen in 2nd half of night.
Sleepwalking triggers?: Sleep deprivation, fevers, meds (lithium, phenothiazenes [compazine, thorazine], tricyclics).
Reasons to get sleep study in suspected parasomnia?: Injury, medico-legal issues, high frequency of events, daytime somnolence.
Prevalence of bruxism over age 60? In kids?: About 3%. 20-88% of kids.
Usual rate of bruxism?: About 1 per second.
Appropriate paper speed for examining rhytmic EEG activity?: 30mm/sec (10 second epoch)
Probablility of seizure in REM, NREM, wake.: NREM > Wake > REM
Mimics of spike and wave?: Bursts of theta or delta (no spikes); electrode popping (usually slower frequency than spike and wave).
Difference between interictal spike and wave activity versus ictal (or seizure) activity?: Interictal is isolated. Ictal occurs in bursts.
Percentage of seizure occuring primarily or only in sleep?: 10-40%
Insomnia at home, but relatively normal sleep in the lab or when away from home?: Psychophysiological insomnia.
Psychophysiological insomnia of less than 6 months?: Adjustment sleep disorder
Three GABA-benzo receptor subtypes, BZ1, 2, and 3. Which is responsible for hypnotic effect?: BZ-1.
BZ-2 and -3 induce muscle relaxant, anti-seizure and anxiolytic effects.
Presentation of delayed sleep phase syndrome?: Sleep onset insomnia.
Two antidepressants that increase REM sleep?: Bupropion and nefazodone.
Mechanism of mirtazapine?: Blocks 5HT-2, 5HT-3, histamine type 1, alpha-2 receptors.
Kleine-Levin syndrome?: Recurrent hypersomnia. At leas 1-2 times per year, 3-21 day episode of voracious appetite, hypersexuality, disinhibition. Can just be hypersomnolence.

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