wk 10 BB Flashcards

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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
25
Q

As Fatal Famillial Insomnia progesses, it affects

EEG shows

what happens to sleep scycle

Final symptoms

A

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
Q
A