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Nervous System IV > Sleep, Attention, & Consciousness > Flashcards

Sleep, Attention, & Consciousness Flashcards

1
Q

Effects of ACh on sleep

A

Muscarinic agonists and AChEIs activate REM

Antimuscarinic drugs cause drowsiness but decrease REM

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2
Q

Effects of histamine on sleep

A

Histamine inhibits the REM-ON switch promoting wakefulness

Antihistamines promote drowsiness and sleep

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3
Q

Effects of adenosine on sleep

A

Accumulation of adenosine signals time to sleep

Adenosine antagonists (caffeine) increases alertness

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4
Q

Mechanism of Benzo action in sleep

A

Agonists at GABA-A1 receptors in the cortex which mediate sleep, amnestic, and anticonvulsant actions

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5
Q

Benzodiazepines used for sleep + Pharmacokinetics

A

Triazolam - short half-life; good effect on sleep latency, can see rebound insomnia next day

Temazepam - medium half-life; minimal effect on sleep latency due to slow absorption

Flurazepam - long half-life with active metabolite; can accumulate in elderly due to impaired hepatic clearance

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6
Q

Adverse effects of benzodiazepines in sleep

A

Daytime sedation
Anterograde amnesia
Rebound insomnia
Psychologic and physical dependence (Schedule IV)

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7
Q

Benzodiazepines vs. Z drugs

A

Both decrease sleep latency, increase sleep duration with increased Phase 2 (light sleep)

Most benzos, barbiturates, and ethanol decrease phase 3-4 deep sleep and REM with REM rebound leading to nightmares; Z drugs have minimal effect on sleep architecture

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8
Q

Treatment of benzodiazepine overdose

A

Flumazenil

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9
Q

Ramelteon

A

Melatonin (MT1 and MT2) receptor agonist - induces sleepiness and regulation of circadian rhythms via SCN of hypothalamus

Reduces sleep latency time - good treatment of insomnia characterized by difficulty with sleep onset

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10
Q

Trazodone

A

Serotonin antagonist / reuptake inhibitor (SARI)

Uses: Patients with co-morbid substance abuse/depression

Adverse effects: Orthostasis, Priapism

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11
Q

Use of TCADs in insomnia

A

Block reuptake of 5HT and NE; antagonist action at histamine and muscarinic cholinergic receptors

Option for insomnia patients with co-morbid depression and substance abuse

Adverse reactions: Anticholinergic / antihistaminic side effects; cardiac conduction disturbances in overdose

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12
Q

Diphenhydramine

A

Histaminic and muscarinic antagonist; produces drowsiness

Not indicated for use in insomnia

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13
Q

Characteristics of Z drugs

A

1st line therapy for insomnia

Little effect on sleep stages III, IV, and REM
Negligible anticonvulsant or myorelaxant properties at therapeutic doses
Low tolerance and abuse potential

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14
Q

Z Drug Adverse Effects

A

Drowsiness, amnesia, headache, GI complains

Rebound effects or next-day psychomotor performance alteration minimal with Zolpidem and Zaleplon, increased with Eszopiclone

Tolerance, dependence, withdrawal are possible but less likely than with benzodiazepines; still schedule IV

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15
Q

What are the 3 types of ADHD?

A

Inattention type, characterized by inability to initiate, maintain, shift, or terminate attention

Hyperactive/Impulsive Type

Combined inattention/hyperactive type

All types require evidence of impairment before age 12 with symptoms present in at least 2 settings

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16
Q

What is the epidemiology of ADHD?

A

3-8% of school-aged children
4% of adults

Males > Females

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17
Q

What is the role of psychiatric comorbidity in ADHD?

A

65% of children with ADHD experience psychiatric comorbidity, including:

Major depression
Anxiety / social phobia
Oppositional / conduct disorder
Antisocial personality disorder 
Substance abuse
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18
Q

Stimulant treatments for ADHD

A

Methylphenidate derivatives - Focalin/Ritalin (short acting) vs. Concerta (long acting)

Amphetamine salts - Adderall (short acting)

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19
Q

Non stimulant-based treatment of ADHD

A

NRIs (Atomoxetine)
NDRIs (Buproprion)
TCADs
Alpha-agonists (Clonidine) - for hyperactivity

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20
Q

Delirium

A

A state of fluctuating confusion, inattention, and misperceptions (illusions/hallucinations)

21
Q

Stupor

A

A sleep-like state from which the patient can be aroused only by vigorous stimuli

22
Q

Coma - Definition

A

A sleep-like state in which the patient is unresponsive to external stimuli and there are no sleep-wake cycles or attempts to communicate

Defined as GCS < 8; patients are unable to follow commands, speak recognizable words, or open either eye

23
Q

Vegetative State - Definition

A

Eyes open spontaneously, sleep-wake cycles re-establish, but there is no sign of cognitive function (perception, communication, or purposeful motor activity)

Persistent VS = duration 1 month
Permanent VS = duration 3 months (non-traumatic) or duration 12 months (traumatic)

24
Q

Minimally conscious state (MCS)

A

Eyes open spontaneously and sleep cycles resume; arousal level may be normal at times with reproducible, though inconsistent, behavioral displays of perception, communication, or purposeful motor activity

25
Q

Decerebrate posturing

A

Upper and lower extremity extension
Suggests lesion of upper brainstem
Worse prognosis than decorticate

26
Q

Decorticate posturing

A

Upper extremity flexion with lower extremity extension

Suggests lesion of cerebral hemisphere

27
Q

Components of brain death

A
  1. Unresponsiveness / Deep Coma (GCS = 3)
  2. No cerebrally modulated motor response to painful stimuli (spinal reflexes may be present; seizures or flexor/extensor posturing may NOT)
  3. All brainstem reflexes are absent (pupils, corneals, oculovestibular, oculocephalic, gag, cough, respiratory effort)
  4. Core body temperature of 32.2 (90F)
  5. Toxicology is non-explanatory
  6. Adequate BP (SBP > 90) and pulse (>50)
28
Q

Stage 1 Sleep

A

Transition phase with EEG similar to wakefulness

29
Q

Stage 2 Sleep

A

Light sleep

Accounts for 50% of total sleep

30
Q

Stages 3 and 4 Sleep

A

EEG is very slow; deepest level of sleep

Disorders of arousal (sleep walking and night terrors) occur during Stages 3 and 4 sleep, earlier in the night

31
Q

REM Sleep

A

Cycles occur every ~90 minutes, concentrated toward the later part of the night

EEG looks awake but arousal threshold is higher than in SWS; muscles are paralyzed except for eyes and diaphragm, heart beats and respirations are irregular

REM behavior disorder occurs

32
Q

Delayed sleep phase syndrome

A

Misalignment of alerting system with social demands;

Larks want to sleep and wake early; if remain awake late, wake early resulting in EDS

Night owls want to sleep late and wake late; experience EDS when awakened before alerting rhythms rise

33
Q

Insomnia - Contributing factors

A

Predisposing factors: Anxiety, worry, moodiness

Precipitating factors: Anything causing a sleepless night

Perpetuating factors: Catastrophizing about sleep, self-medication with ETOH and drugs

34
Q

Restless Leg Syndrome

A

Primary RLS is due to DA abnormalities and can be worsened by psychotropic medications (SSRIs, TCAs, Lithium) and antihistamines

Increased risk with iron deficiency anemia (ferritin replacement if < 55)

35
Q

REM Behavior Disorder

A

Failure of skeletal muscle inhibition during REM leads to acting out dreams

Treatment: Clonazepam, Melatonin

36
Q

Narcolepsy

A

EDS followed by cataplexy

Cataplexy = short, sudden episode of lost muscle tone triggered by emotion; varies from slight facial weakness to total collapse

37
Q

Excessive Daytime Sleepiness - DDx

A

High Epworth score due to:

Insufficient sleep / poor sleep habits
Circadian rhythm disorders - delayed sleep phase, shift-work, jet lag 
Sleep apnea
Narcolepsy
Idiopathic hypersomnia 
Drug use / withdrawal
Restless leg syndrome
38
Q

Fatigue - DDx

A

Low Epworth score due to:

Anxiety
DepressionConditioned / learned insomnia

39
Q

How do we ‘entrain’ to a 24 hour day?

A

Morning light from the retina travels to the SCN via the RHT; SCN signals the pineal gland and inhibits production of melatonin

In the absence of light this inhibition is removed, melatonin is constitutively produced, and people will “free run” on a 24.2 hour day

40
Q

How is sleep and wakefulness regulated by temperature?

A

Sleep is best on the descending curve of core body temperature; awakening occurs spontaneously 2-3 hours after body temperature begins to rise

41
Q

Zolpidem

A

Most widely prescribed hypnotic agent

Effective for reducing sleep latency and nocturnal awakenings due to rapid oral absorption and short half-life; increases total sleep time and efficacy

42
Q

Zaleplon

A

Effective for decreasing sleep latency; NOT effective for preventing nighttime awakenings or increasing total sleep time

Best for use in treatment of night time awakenings; can get the patient back to sleep (rapid onset) but eliminated by morning with little hangover (short half life)

43
Q

Eszoplicone

A

Longer half life Z drug agent; relatively safer for long term use without development of tolerance, dependence, or abuse

44
Q

Which region of the brain is the sleep/wake switch?

A

Hypothalamus

45
Q

Which region of the brain is the NREM/REM switch?

A

Brainstem

46
Q

Narcolepsy

A

Patients have reduction in the number of hypocretin / orexin neurons, which destabilizes the sleep/wake switch

Patients experience unwanted transitions into sleep during wakefulness as well as frequent periods of awakening during sleep; patients quickly enter REM sleep at any time and experience REM-like episodes such as loss of muscle tone while awake (cataplexy)

Treat with naps, stimulants, Na oxybutyrate

47
Q

Pathophysiology of Narcolepsy

A

Normally, hypocretin-secreting neurons activate serotonergic, noradrenergic, and histaminergic neurons that inhibit the “REM-ON” switch, promoting wakefulness; loss of hypocretin-secreting cells may disinhibit the REM-ON switch

48
Q

Effects of 5HT and NE on sleep

A

5HT and NE inhibit the REM-ON switch promoting wakefulness

SSRIs, SNRIs and TCADs suppress REM sleep

49
Q

Normal sleep pattern

A

50% Stage 2 Sleep
25% Slow Wave Sleep (NREM Stages 3 and 4)
25% REM

Minimal sleep latency, minimal nocturnal awakenings

Nervous System IV (10 decks)

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