wk 10 BB Flashcards

1
Q

SCN is located in the

A

hypothalamus

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2
Q

lesions in SCN do what to sleep

A

still sleep and exercise normal ammount, just at haphazard times

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3
Q

greater SCN neuronal and metabolic activity during

A

daylight

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4
Q

light passes directly from the retina to the SCN via the

A

Retinohypothalamic pathway

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5
Q

how does the SCN control sleep and waking through Direct neural connections

process of SCN to DMH

A

synapse pathways from SCN to the
- subparaventricular zone (SPZ)
-then to Dorsomedial nucleus of the Hypothalamus (DMH)

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6
Q

how does the SCN control sleep and waking through Direct neural connections

process of DMH to sleep-wake flip-flop

A
  • DMH sends inhibitory signals to vlPOA (GABAnergic system here) which is inhibitory, thus keeping us awake

DMH sends excitatory signals to Oxinergic neurons ( excitatory, this promotes wakefulness) (as oxinergic neurons stimulate arousal system)

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7
Q

evidence that the SCN control sleep and waking through release of chemical signals

A

system involving at least 7 genes and their proteins and two interlocking feedback loops.
– Proteins build up, inhibit gene producing proteins. Proteins lessen, stop inhibiting, proteins produced.

a biological clock

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8
Q

Insomnia

A

difficulty getting to sleep, staying asleep, or having non-restorative sleep

– together with associated impairment of daytime functioning.

– Defined in relation to a person’s
particular need for sleep

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9
Q

Chronic insomnia effects
approximately __% of the population
while up to 1/3 report at least one
nocturnal symptom (Morin & Jarrin, 2013;
Singareddy et al., 2012).

A

9

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10
Q

insomnia

Age
– More common in ____ people

A

older

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11
Q

Causes for insomnia = Physiology

A

Heightened activity in the reticular activating system

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12
Q
  • Medical conditions and medications
    impact on insomnia
A

E.g. Heart and respiratory conditions, some
antidepressants, epilepsy medications

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13
Q

Insomnia Treatment

A

Typically treated with drugs but can
potentially also be treated with
mindfulness and CBT (Manber et al.,
2011; Ong et al., 2014)

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14
Q

Chronic sleep deprivation can lead
to serious health problems e.g.

A

E.g. obesity, diabetes and
cardiovascular disease (Orzel-Gryglewska,
2010)

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15
Q

Sleep Apnea

A

Form of insomnia – the inability to
sleep and breathe at the same time
* Build of carbon dioxide
* Carbon dioxide in the blood
stimulates chemoreceptors
* Disrupts sleep affecting daytime
functioning

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16
Q

Narcolepsy

Symptoms

A

Sleep attack = overwhelming urge to sleep

Cataplexy = muscular paralysis of REM sleep while awake

Varying degrees of muscle weakness
➢ Can become completely paralyzed while conscious
➢ Generally occurs when the person feels strong
emotions or by sudden physical effort.

Sleep paralysis =
* REM muscular paralysis just before the onset
of sleep or upon waking

Hypnagogic hallucinations =
* dreaming while awake and paralysed
* can very realistic and terrifying.

17
Q

Causes of narcolepsy

A

Hereditary element

Environmental factors play, but are unknown

Orexinergic neurons are attacked by the
immune system, usually in adolescence
(Fontana et al., 2010)

18
Q

treatments for narcolepsy

A

Ritalin - stimulant drugs.

REM sleep phenomenon treated with antidepressants

most common = modafanil and sodium oxybate

19
Q

REM sleep behaviour disorder

A

no paralysis during REM

= acting out dreams

Neurodegenerative disorder with a genetic component

associated with Neurodegenerative disorders such as Parkinsons

20
Q

REM sleep behaviour disorder treatment

A

clonazepam , a benzodiazepine tranquilliser

21
Q

Sleepwalking (somnambulism)

slow-wave sleep problem

A

different to acting out dream but can engage in complex behaviours

more common in children

Genetic component

22
Q

Night terrors

A
  • Night terrors (pavor nocturnus)
    ➢ Anguished screams, trembling, a rapid pulse, and usually
    no memory of what caused the terror
    ➢ Hereditary element
23
Q

Bedwetting (nocturnal enuresis)

A

➢ About 10% of 7 year olds
➢ Heredity element

24
Q

Fatal Familial Insomnia

A

Neurodegenerative condition
* Prion disease
* Damage to the thalamus

Initially presents with insomnia and very vivid dreams when the person finally manages to sleep.

  • Psychiatric complications – panic attacks, cognitive deficits, paranoia and phobias
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As Fatal Famillial Insomnia progesses, it affects EEG shows what happens to sleep scycle Final symptoms
the autonomic nervous system (e.g. elevated blood pressure) and coordination (ataxia) disturbances and reductions in sleep spindles and K complexes Dissapearance of slow wave sleep and only brief periods of REM sleep Ultimately leads to inability to speak or move (akinetic mutism), coma and death
26