10 Sleep 2

Question 1

Q: What are circadian rhythms?

Answer 1

A: Circadian rhythms are patterns of change in behavior or physiological processes that follow a daily rhythm, generally aligned to changes in illumination.

Question 2

Q: How does the internal clock function in the absence of light stimulation?

Answer 2

A: The internal clock runs to approximately 25 hours in the absence of light stimulation.

Question 3

Q: What are zeitgebers, and how do they synchronize circadian rhythms?

Answer 3

A: Zeitgebers are time-givers that synchronize circadian rhythms. Fluctuations in light are a primary zeitgeber, keeping the clock to a 24-hour cycle.

Question 4

Q: How does artificial light affect the biological clock?

Answer 4

A: Artificial light can delay the biological clock, but the clock still runs to a 25-hour cycle regardless of light exposure.

Question 5

Q: What is the suprachiasmatic nucleus (SCN) and its role in circadian rhythms?

Answer 5

A: The SCN, located in the hypothalamus, is the primary control center of circadian rhythms. Lesions to the SCN result in randomly dispersed bursts of sleep, indicating its importance in maintaining rhythmic activity.

Question 6

Q: How does light serve as a zeitgeber in mammals?

Answer 6

A: Light sets the circadian rhythm by passing directly from the retina to the SCN via the retinohypothalamic pathway.

Question 7

Q: What are the two ways the SCN controls sleep/waking?

Answer 7

A: The SCN controls sleep/waking through direct neural connections and the release of chemical signals.

Question 8

Q: How does the SCN influence sleep/waking through direct neural connections?

Answer 8

A: The SCN sends synapse pathways to the subparaventricular zone (SPZ) and dorsomedial hypothalamus (DMH), which then connect to regions involved in the control of sleep and waking, such as the ventrolateral preoptic area (vlPOA) and orexinergic neurons.

Question 9

Q: What happens during the day in terms of sleep/waking regulation by the SCN?

Answer 9

A: During the day, the DMH inhibits the vlPOA and excites brain stem and forebrain arousal systems, stimulating wakefulness.

Question 10

Q: What evidence supports the role of the SCN in controlling sleep/waking through chemical signals?

Answer 10

A: Destroying the SCN abolishes circadian rhythms, and transplanting donor tissues can restore rhythms, even when the tissue is prevented from creating new synaptic connections. This suggests that chemicals secreted from the SCN affect the rhythms of sleep and waking.

Question 11

Q: What is the nature of the circadian clock?

Answer 11

A: The circadian clock involves at least seven genes and their proteins, forming two interlocking feedback loops. Proteins in the first loop reach a sufficient level to trigger the second loop, resulting in a cycle of production and degradation of these proteins. Mutations in these genes can lead to sleep disorders such as advanced sleep phase syndrome or delayed sleep phase syndrome.

Question 12

Q: How can shift work and jet lag affect circadian rhythms?

Answer 12

A: Changes in the daily rhythms of activity, such as those caused by shift work or jet lag, can disrupt the synchronization between internal rhythms and the external environment. This disparity can negatively affect functioning, leading to accidents related to sleepiness, which are more common in individuals with irregular working patterns.

Question 13

Q: How does jet lag typically resolve, and what methods can help overcome its effects?

Answer 13

A: Jet lag typically resolves over a few days. Methods to overcome its effects include exposure to bright light at appropriate times, maintaining bright artificial light and dark bedrooms, and using bedtime melatonin supplements. Melatonin can affect the sensitivity of SCN neurons to zeitgebers and alter circadian rhythms.

Question 14

Q: What are the DSM-V criteria for insomnia?

Answer 14

A: Insomnia is characterized by difficulty getting to sleep, staying asleep, or experiencing non-restorative sleep, along with associated impairment of daytime functioning. It is defined in relation to a person’s particular need for sleep.

Question 15

Q: What percentage of the population does chronic insomnia affect, and what are some common causes?

Answer 15

A: Chronic insomnia affects approximately 9% of the population, with up to one-third reporting at least one nocturnal sleep disturbance. Causes may include age-related factors, environmental factors such as electronic devices, noise, and light, heightened activity in the reticular activating system, changes in circadian rhythms, and medical conditions or medications.

Question 16

Q: How is sleep apnea characterized, and what physiological mechanisms are involved?

Answer 16

A: Sleep apnea is characterized by the inability to sleep and breathe at the same time. It can lead to disruptions in sleep and affect daytime functioning due to the buildup of carbon dioxide in the blood stimulating chemoreceptors.

Question 17

Q: What are some treatments for sleep apnea?

Answer 17

A: Sleep apnea caused by obstruction can be corrected surgically or relieved by pressurized air that keeps the airway open, such as continuous positive airway pressure (CPAP) therapy.

Question 18

Q: What are the symptoms of narcolepsy?

Answer 18

A: Symptoms of narcolepsy include sleep attacks (overwhelming urge to sleep), cataplexy (muscular paralysis of REM sleep while awake), varying degrees of muscle weakness, complete paralysis while conscious, sleep paralysis (REM muscular paralysis just before onset of sleep or upon waking), and hypnagogic hallucinations (dreaming while awake and paralyzed, often realistic and scary).

Question 19

Q: What are some common treatments for narcolepsy?

Answer 19

A: Treatments for narcolepsy may include the use of stimulants such as methylphenidate to diminish sleep attacks, antidepressant drugs to manage REM sleep phenomena, and stimulant drugs like modafinil and sodium oxybate.

Question 20

Q: What are the potential causes of narcolepsy?

Answer 20

A: Narcolepsy has a hereditary component, and environmental factors may also play a role, although they are not fully understood. It is believed that orexinergic neurons are attacked by the immune system, typically during adolescence.

Question 21

Q: What is REM sleep behavior disorder (RBD)?

Answer 21

A: REM sleep behavior disorder is characterized by a failure to exhibit paralysis during REM sleep, leading to acting out dreams. It is a neurodegenerative disorder with a genetic component and is associated with other neurodegenerative conditions like Parkinson’s disease.

Question 22

Q: How is REM sleep behavior disorder typically treated?

Answer 22

A: REM sleep behavior disorder is usually treated with clonazepam, a benzodiazepine tranquilizer.

Question 23

Q: What is sleepwalking, and who is more prone to it?

Answer 23

A: Sleepwalking involves engaging in complex behaviors while asleep, without acting out dreams. It is more common in children and has a genetic component. Sleepwalking is considered a disorder of arousal.

Question 24

Q: What are night terrors, and what are their characteristics?

Answer 24

A: Night terrors are episodes characterized by screams, trembling, and a rapid pulse, usually without any memory of the events. There is a hereditary element associated with night terrors.

Question 25

Q: What is bedwetting, and what percentage of 7-year-olds are affected by it?

Answer 25

A: Bedwetting, or nocturnal enuresis, is the involuntary release of urine during sleep. It affects approximately 10% of 7-year-olds and has a hereditary component.

Question 26

Q: What is fatal familial insomnia, and what are its symptoms?

Answer 26

A: Fatal familial insomnia is a neurodegenerative disorder and prion disease characterized by damage to the thalamus. Symptoms initially include insomnia and vivid dreams upon falling asleep. As the disease progresses, it can lead to psychiatric complications such as panic attacks, cognitive deficits, paranoia, and phobias. It also affects the autonomic nervous system, leading to elevated blood pressure and coordination issues. EEG shows disturbances and reductions in sleep spindles and K complexes, with the disappearance of slow-wave sleep and only brief periods of REM sleep. Ultimately, it results in an inability to move or speak voluntarily, coma, and death.