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Neuro Week 6 > ICL 10.12: Sleep, Wakefulness & Disorders > Flashcards

ICL 10.12: Sleep, Wakefulness & Disorders Flashcards

1
Q

what are the 4 arousal mechanisms in our brain?

A
  1. Ascending Reticular Activating System (ARAS)
  2. Lateral Hypothalamus
  3. Tuberomammillary Nucleus
  4. Basal Forebrain

ARAS is the main activating system while the lateral hypothalamus and tuberomammilary nucleus are part of the hypothalamus and feed into the ARAS pathway

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2
Q

what is the pathway of the ascending reticular activating system?

A

it’s loosely arranged neurons that start in the brainstem and then ascend to the diencephalon and then to the cortex causing activation of the cortex and hence arousal

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3
Q

what are the two divisions of the ascending reticular activating system?

A
  1. dorsal
  2. ventral

dorsal RAS from Lateral Dorsal Tegmental (LDT)/Pedunculopontine Tegmentum (PPT) –> REM-on and REM & wake-on neurons –> thalamus (medial and intralaminar nuclei)/ LH/midbrain –> activate cortex

ventral RAS projects from Dorsal Raphe Nucleus (5HT) and Locus Coeruleus (NE), through the lateral hypothalamus terminating on Basal forebrain –> cortex

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4
Q

what are the 5 nuclei that feed into the ascending reticular activating system?

A
  1. locus coeruleus
  2. dorsal raphe nucleus
  3. tuberomammilary nucleus (TMN)
  4. lateral hypothalamus (LH)
  5. substantia nigra
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5
Q

what is the role of the locus coeruleus in the ARAS? what does it secrete?

A

a nuclei in the pons composed of neurons in the dorsal brainstem that secretes norepinephrine

it feeds into the ventral ARAS

norepinephrine is important in mood and autonomic neurosystem functions like BP and heart rate –> your state of arousal is also determined by norepinephrine

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6
Q

what is the role of the dorsal raphe nucleus in the ARAS? what does it secrete?

A

a nucleus in the rostral brainstem and pons that secretes serotonin

it feeds into the ventral ARAS

serotonin is important for regulating mood and keeping us awake – so when 5HT levels are low people are depressed and drowsy

SSRIs act on the dorsal raphe nucleus to increase the levels of serotonin!

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7
Q

what is the role of the tuberomammilary nucleus in the ARAS? what does it secrete?

A

part of the hypothalamus that feeds into the ventral ARAS even though it’s not directly part of ARAS

it secretes histamine which is important in arousal

when you take anti-histamines which block histamine, you get drowsy because histamine is blocked in the TMN! also nyquil is an anti-histamine and that’s why it helps you fall asleep!

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8
Q

what is the role of the lateral hypothalamus in the ARAS? what does it secrete?

A

part of the hypothalamus that feeds into the ventral ARAS even though it’s not directly part of ARAS

it makes and secretes orexin aka hypocretin (there’s orexin A and B)

orexin is a really long peptide in comparison to the other NTs which are made out of single amino acids! it’s longer, heavier and bigger and it’s extremely important!!

orexin A is important for maintaining arousal and weight regulation –> so people low on orexin will either be sleepy or gain a bunch of weight

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9
Q

what is the role of the substantia nigra in the ARAS? what does it secrete?

A

neurons in the midbrain which contains dopamine cells and feed into the ventral ARAS

dopamine is important for motor execution –> low dopamine means Parkinsonism

dopamine is also important for arousal –> low dopamine means sleepiness!

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10
Q

what are the 2 nuclei in the dorsal ARAS?

A
  1. peduncular pontine nucleus (PPT)

2. lateral dorsal tegmental nucleus (LDT)

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11
Q

what is the role of the PPT and LDT in the ARAS?

A

they are nuclei in the midbrain which feeds into the dorsal ARAS (LDT is a little more rostral)

both secrete ACh which feeds into the medial and intralaminar nuclei of the thalamus and then to the cortex to cause arousal!

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12
Q

what’s the difference between the function of the dorsal vs. ventral nuclei of the ARAS?

A

the dorsal nuclei (LDT and PPT) are important for arousal but also for sleep!!

they have 2 populations of neurons:

the first is wake-on which means they’re on only during the wake stage

the other is REM-on which means they’re functional during REM sleep

so LDT and PPT are important for awake and REM sleep!

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13
Q

antihistamines act on what part of the ARAS?

A

they antagonize the histamine receptors in the tuberomammilary nucleus (TMN) of the hypothalamus

ex. benadryl and cetirizine

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14
Q

stimulants act on what part of the ARAS?

A

they act on the dopamine centers in the substantia nigra of the midbrain

stimulants increase the levels of dopamine which causes arousal – sometimes there’s too much arousal which causes insomnia and psychosis

ex. amphetamine, MDMA, meth

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15
Q

antidepressants act on what part of the ARAS?

A

they can act on either one or both the dorsal raphe nucleus to increase serotonin and the locus coeruleus to increase NE

by increasing 5HT or NE in the synapses, symptoms of depression are improved

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16
Q

anticholinergics act on what part of the ARAS?

A

ACh is important for maintaining arousal so anticholinergics can cause confusion, delirium

ex. atropine, 1st generation antidepressants

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17
Q

what are the side effects of atropine?

A

atropine is an anticholinergic that acts on the lateral dorsal tegmental nucleus and pedunculopontine nucleus in the dorsal ARAS

mad as a hatter, dry as a bone, blind like a bat and red like a beat = side effects of atropine

so they’ll be crazy from decreased ACh which normally maintains arousal, they’ll be dry from decreased mucous secretion and no sweating, blind because they have small pupils, and red because they’ll be flushed

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18
Q

what is the function of the basal forebrain in the ARAS?

A

the basal forebrain is small areas of grey matter in the forebrain inferior to the basal ganglia which contain cholinergic neurons that secrete ACh

ACh will then disinhibit cortical pyramidal cells through GABA and cause arousal

it’s important because the ventral ARAS will feed into the basal forebrain before it then projects diffusely to the rest of the cortex

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19
Q

what part of the forebrain is effected in Alzheimer’s patients?

A

basal nucleus of Meynert in the basal forebrain

it’s one of the nuclei in the basal forebrain that secretes ACh which is important in both arousal and cognition

so patients who have AD dementia lose neurons in this nucleus of the forebrain!

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20
Q

which 5 nuclei in the hypothalamus are important for sleep/arousal?

A
  1. paraventricular nucleus

important for maintaining timing of sleep

  1. lateral nucleus

secretes orexin which keeps you awake

  1. tuberomammillary nucleus

secretes histamine which keeps you awake

  1. superchiasmatic nucleus

biologic clock that maintains most circadian rhythms in your body including sleep

  1. ventrolateral preoptic nucleus (VLPO)

secretes GABA

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21
Q

what is the clinical presentation of someone with a lesion in the caudal brain stem vs. rostral brainstem vs. cortex?

A

cortex lesion = impaired awareness like a vegetative state –> can breathe, swallow, sleep, wake, but no meaningful response to external stimuli

rostral brainstem/thalamus lesion = impaired arousal like in a coma

caudal brainstem lesion = brain death, not compatible with life because the respiratory and cardiovascular centers in the medulla are involved

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22
Q

which part of the ARAS is most involved with narcolepsy with cataplexy?

A

the lateral hypothalamus which secretes orexin A and B

LH secretes orexin which then activates all the parts of the dorsal and ventral ARAS = TMN, substrata nigra, dorsal nucleus of raphe, locus coeruleus, PPT and LDT

in narcolepsy with cataplexy, here is loss of over 90% of orexin-secreting neurons in the lateral hypothalamus

but in narcolepsy without cataplexy, there’s only partial loss of these neurons

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23
Q

which orexin is more clinically important?

A

hypocretin 1/orexin A because it binds to both Hcrt1 and Hcrt2 receptors

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24
Q

what is the rate of orexin neuron firing in exploring, grooming, eating, NREM and REM?

A

the rate of orexin firing neurons in the lateral hypothalamus is as follows during various activities:

engaging behaviors > grooming/eating&raquo_space; quiet wake&raquo_space;» NREM, REM

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25
Q

where is the ventrolateral preoptic nucleus located and what NTs does it secrete?

A

it’s one of the hypothalamic nuclei

it secretes GABA and galanin which are both inhibitory

it’s important for sleep!

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26
Q

how is sleep induced via the ventrolateral preoptic nucleus?

A

the ventrolateral preoptic nucleus in the hypothalamus secretes GABA and galanin and inhibits all of the ARAS = TMN, RN, LC, SN, PPT, and LDT

adenosine, PGD2 and warmth activate the VLPO which then secretes GABA/galanin to shut everything else down

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27
Q

levels of what NT are high when you are tired?

A

adenosine

coffee contains caffeine and what it does it block adenosine receptors and help you stay awake by blocking the effects of adenosine on VLPO (ventrolateral preoptic nucleus of the hypothalamus)

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28
Q

how does the sleep-wake switch work?

A

AWAKE
when you’re awake the orexin neurons and ARAS neurons (LDT, PPT, LC, RN, TMN) are active

the preoptic nucleus is relatively inactive

so the orexin and wake-active neurons are dominating and inhibiting the VLPO nucleus so the person is awake

SLEEP
the VLPO is more active and it’s inhibiting both the orexin neurons and the wake-active neurons so the person will be asleep

so it’s all a tug-o-war between the VLPO vs. the orexin neurons and wake-active neurons of the ARAS

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29
Q

what are the 2 stages of sleep based on EEG?

A
  1. NREM = non-rapid eye movement
  2. REM = rapid eye movement –> aka paradoxical sleep

NREM is also called slow wave sleep and it more refreshing

REM is less refreshing/more active dreaming –> metabolic activity of the brain is really high so that’s why you aren’t as relaxed

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30
Q

what are the stages of NREM?

A

there are 3 progressively slower stages = N1, N2 and N3

N1 to N3 is a progression into the deeper stages of sleep

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31
Q

4 sleep waveforms seen on EEG?*

A

they are based on frequency

  1. beta = 14-30 Hz –> awake, normal alert consciousness, thinking
  2. alpha = 9-13 Hz –> awake, relaxed, calm, lucid, not thinking
  3. theta = 4-8 Hz –> deep relaxation and meditation, mental imagery, maybe drowsy
  4. delta = 1,3 Hz –> deep, dreamless sleep

so as the frequency increases, amplitude decreases – as the frequency decreases the amplitude increases

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32
Q

what waveforms will you see during the progression of someone being awake to them being asleep?

A

BATS Drink Blood

Beta rhythm –> awake

Alpha rhythm –> drowsy

Theta rhythm –> stage N1 of NREM

Spindles and K complexes –> stage N2 of NREM

Delta rhythm –> stage N3 of NREM

Back to Beta –> awake

so now you’re asking what about REM sleep?? well REM sleep is basically low amplitude alpha, it’s very similar to an awake state which is why it’s called paradoxical sleep

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33
Q

what are sleep spindle and K complexes?

A

sleep spindles are faster 12-14 Hz so almost alpha rhythms with a crescendo then decrescendo pattern

K complex is a biphasic high amplitude discharge that goes up then down – looks like a heart rhythm – normally seen in the front of the brain

these are the 2 phases of stage N2 NREM sleep and they come from the reticular thalamic nucleus!

slide 28 and 29 (go look seriously)

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34
Q

what wave forms are considered one sleep cycle?

A

going from beta to delta is one sleep cycle

during sleep, you go from beta to delta multiple times and keep repeating

each cycle takes 90-100 minutes but usually an adult goes through 4-5 sleep cycles a night

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35
Q

what is REM sleep?

A

also called paradoxical sleep, due to loss

of muscle tone except in extraocular muscles and diaphragm

36
Q

what are the 2 phases of REM sleep?

A
  1. tonic stage

2. phasic stage

37
Q

what happens during the tonic stage of REM sleep?

A
  1. EEG low amplitude
  2. suppression of muscle tone except EOM and diaphragm
  3. absent thermoregulation = become cold blooded
  4. penile/clitoral erections
  5. pupils constrict (due to parasympathetic dominance)
38
Q

what happens during the phasic stage of REM sleep?

A
  1. contraction of middle ear muscles
  2. irregular respiration and heart rate
  3. rapid eye movements

these happen only intermittently throughout REM, not during all of REM sleep – most of REM sleep is the tonic phase

39
Q

why is there loss of muscle tone during REM sleep?

A

the PPT and LDT nuclei have REM-on neurons which are inhibited during wake-stage by the ARAS components

in the sleep state, the ARAS nuclei are shut down so the inhibition on the PPT and LDT REM-on neurons is lifted and they are dis-inhibited during sleep –> VLPO is what switches off the ARAS components

when they are disinhibited they become active and release ACh which activates the medial medullar nucleus in the medulla which inhibits the motor neurons in the spinal cord

this is why when you’re dreaming about running you aren’t actually running in your bed!

40
Q

what happens to the amount of N3 NREM sleep throughout the night?

A

N3 sleep becomes less prevalent as you go through the night

so you don’t sleep as deep towards the end of the night

as the N3 decreases, your REM increases which is why we dream a lot towards the end of the night and early morning and remember those dreams when we get up

41
Q

what does it mean if someone goes directly into REM sleep after falling asleep?

A

it’s super unusual for a healthy person to go straight into REM without going through N1 –> N3 first

if someone does go straight into REM it usually indicates depression or narcolepsy

however, awake directly into REM in babies is totally normal

42
Q

what is a hypnogram?*

A

the depiction of sleep stages vs. time

slide 31

43
Q

what stage of sleep do you spend most of your time in?

A

N2

50-60% of your sleep is in N2

44
Q

what is the difference between REM and non-REM eye movement, body movement, vital signs, muscle tone, penile erection, dreams, and EEG?

A

REM SLEEP
rapid eye movement

muscle twitches

fluctuating vital signs

decreased muscle tone

penile erections are common

dreams are common

EEG is low voltage, high frequency alpha waves

NON-REM SLEEP
slow eye movements

muscle relaxation but not totally atonic

stable vital signs

some tone in postural muscles

penile erections rare

dreams are rare

EEG has spindles, V-waves, K-complexes and slow waves

45
Q

how much of your sleep is spent in REM vs. non-REM?

A

25-75 REM:non-REM in adults

50-50 in babies

46
Q

what is the opponent model of sleep?

A

it’s what explains circadian rhythmicity!

there are 2 determinants called process S and Process C –> process S makes us tired which process C makes us alert

as we go through the day, process S increases and peaks at 9 PM – but to keep us awake throughout the day, process C is also increasing so it counteracts the effect of the sleep load so you don’t just fall asleep in the middle of the day –> process S and C both peak at 9 PM

the process C signal being generated by the superchiasmatic nucleus in the brain and counteracts sleep load which is adenosine! so the SCN sends out alerting signals throughout the day to counteract rising adenosine signals throughout the day

around 9 PM, your SCN stops sending out alerting signals via process C and you fall asleep because the adenosine sleep load is unopposed (process S)

when you fall asleep, your adenosine decreases over time until you wake up and the sleep load is the lowest in the morning when you get up which is why you’re awake the most in the morning!

slide 34*

47
Q

what are the 3 criteria that a biological rhythm has to meet to be considered a circadian rhythm?

A
  1. rhythm has an endogenous free-running (approximately) 24 h period
  2. should be entrainable (ie, be capable of phase reset by environmental cues and synchronisation to the 24h day like moving from the east coast to the west coast)
  3. should exhibit temperature compensation = temperature doesn’t effect phase of circadian rhythm

If all these criteria are not fulfilled,
the term diurnal rhythm is often used

48
Q

what causes the circadian rhythm of sleep?

A

light activates the suprachiasmatic nucleus of the hypothalamus to activate process C which inhibits melatonin secretion from the pineal gland

so in the day time because of abundant light and SCN activation, melatonin levels are low and that’s why you don’t fall asleep during the day!

once it’s night time and there’s no light, the activation of the SCN decreases so it is no longer inhibiting melatonin release and that’s why you get sleepy in the dark

so light activates the SCN which then inhibits the paraventricular nucleus of the hypothalamus – the PVH is the seat of autonomic function including melatonin secretion so that’s why SCN inhibition of the PVH decreases melatonin levels and keeps you awake –> so process C is actually just a lack of melatonin!!

49
Q

what is the endocrine physiology of sleep?

A
  1. NE, TSH and cortisol are under circadian control and TSH peaks at 2 AM while cortisol peaks at 7 am whether you are sleeping or not
  2. however, GH and PRL are also under circadian control but they ARE sleep controlled so they will be secreted when the person is in slow wave sleep
  3. leptin from the fat which promotes satiety increases during sleep
  4. ghrelin from the stomach which promotes eating decreases during sleep

if someone has sleep loss then your leptin levels will be decreased and ghrelin will be increased and both of them together will lead to excessive eating and weight gain!

sleep loss can also effect growth because GH is released during sleep!

50
Q

A 70-year-old woman presents to the office complaining of poor sleep. She describes trouble falling asleep frequent arousals throughout the night. She states that she can not stop her mind from racing at night. Physical exam is unremarkable. Lab studies are within normal limits.

A

insomnia

51
Q

what is insomnia?

A

sleep difficultyaka difficulty initiating or maintaining sleep, early morning awakening, or both

it is associateddaytime consequencesbecause of night time sleep difficulty, with the supposition that the nighttime or daytime problems are not explained by an inadequate opportunity to sleep

the most common type is Psychophysiological Insomnia, due to anxiety about sleep and heightened arousal when in bed

52
Q

how do you treat insomnia?

A
  1. Cognitive Behavioral Theory (CBT-I)
  2. hypnotic medications –> most act directly or indirectly via GABA

the VLPO turns of all ARAS centers so hypnotic medications act through GABA which is the major NT of the VLPO!

53
Q

where are GABA A vs B receptors found?

A

GABA A is mostly in the brain

GABA B is mostly in the brainstem and spinal cord

54
Q

what is the structure of the GABA(A)receptor?

A

5 subunits which surround a Cl- pore and activation of the receptor leads to influx of Cl- into the neuron –> once Cl- gets into the cell it’s hyperpolarized and inactivated

it has binding sites for various different ligands = GABA and benzodiazepines

GABA binds between the alpha and beta subunits of the receptor

benzodiazepines bind between the alpha and gamma subunits and they do not open the Cl- channel but instead increase the affinity for channel gating by GABA

55
Q

which types of medications can be used for treatment of insomnia?

A
  1. benzodiazepines
  2. non-benzodiazepines
  3. orexin receptor antagonists
  4. melatonin receptor agonists
  5. antidepressants
  6. antihistaminics
56
Q

which drugs are benzodiazepines and what are the side effects?

A
  1. triazolam
  2. estazolam
  3. temazepam

adverse effects = dependence, increased tolerance, and slowed responses

they bind between the alpha and gamma subunits of the GABA(A) receptors and increase the affinity for channel gating by GABA

57
Q

what is the MOA of non-benzodiazepine drugs?

A

they are GABA agonists which bind to the GABA(A) receptor between the alpha and beta subunits on the OTHER side of the receptor, so not at the same binding site as actual GABA

58
Q

which drugs are non-benzodiazepines and what are the side effects?

A
  1. zaleplon
  2. zolpidem
  3. eszopiclone

“the 3 Z’s of sleep!”

adverse effects = less dependence producing than BZD but patients can develop nocturnal eating

59
Q

how do orexin receptor antagonists treat insomnia?

A

orexin is released from lateral hypothalamus and makes you awake

so if you block it you’ll fall asleep

ex. suvorexant (Belsomra)

60
Q

how do melatonin receptor agonists treat insomnia?

A

melatonin binds to superchiasmatic nucleus and turns it off

ex. ramelteon = melatonin 1 and 2 receptor agonist which is 17x more potent than melatonin in binding to the melatonin receptor

61
Q

how do anti-depressants treat insomnia?

A

have some anti-histaminic actions which puts you to sleep because histamine keeps you alert

62
Q

what are interface issues of sleep?

A

there’s either intrusion of sleep into the awake state or intrusion of the awake state into the sleep state

if the switch-model of sleep and wake is unsteady, then the patient might flip from sleep to awake unexpectedly or vice versa –> like with narcolepsy!

63
Q

what are the symptoms of interface issues of sleep?

A
  1. sleep attacks = patients will sleep from sleep to awake rapidly
  2. sleep paralysis (usually due to sleep deprivation)
  3. sleep related hallucinations = hypnogogic and and hypnopompic which is hallucinating when you’re going to sleep or waking up, respectively
  4. cataplexy = loss of muscle tone related to positive or negative emotions
64
Q

what is type 1 narcolepsy?

A

narcolepsy with cataplexy

98% have HLA-DQB1*06:02!!!!

flu or vaccination can also trigger narcolepsy

65
Q

what is type 2 narcolepsy?

A

narcolepsy without cataplexy

about 50% have the HLA-DQB1*06:02

66
Q

what is cataplexy?

A

any emotional trigger which is either positive or negative can trigger a partial cataplexy in the face

eventually they’ll just be down on the ground totally unable to move even though they’ll be totally conscious

67
Q

how do you manage narcolepsy?

A
  1. to treat the excessive daytime sleepiness you can use:

dopamine enhancers like methylphenidate or amphetamine (adderall) but they are dependence producing and can stunt growth in kids

wake promoters like modafinil and armodafinil which are also dopamine enhancers but they can cause headaches

  1. to treat the cataplexy you can use antidepressants or sodium oxybate which is a GABA(B) receptor agonist but it can cause mood changes, bedwetting and sleepwalking
  2. timed daytime naps
68
Q

what are parasomnias?

A

undesirable physical events or experiences that occur during entry to sleep, within sleep, or during arousals from sleep

so it’s when someone goes from sleep to awake unexpectedly

they can occur during REM or non-REM sleep

69
Q

what is a REM sleep behavior disorder?

A

it’s a type of parasomnia so it’s when someone goes from sleep to awake unexpectedly

there’s absence of the normal loss of muscle tone during REM sleep + Dream-enactment behavior (oneirism) –> so when they’re dreaming they’re acting out their dreams!

limb and body movements often are violent (e.g., hitting a wall, kicking) and may be associated with emotionally charged utterances

patientmayormay notremember the dream

pathophysiology includes dysfunction of areas of the brain responsible for atonia during REM sleep and also other areas of the brain (limbic system and others) involved with the generation of the violent dreams

so it’s lack of atonia! the REM-on neurons will inhibit the medulla which inhibits the spinal neurons but without this, that’s why the patient can act out their dream

70
Q

why is REM sleep behavior disorder clinically significant?

A

it’s a prelude to neurodegenetive disorders like Parkinson’s

81% of patients who get diagnosed with RBD later develop Parkinson’s like 10 years later

71
Q

how do you treat REM sleep behavior disorder?

A
  1. patient safety
  2. clonzepam (BZD)
  3. melatonin

besides this there really aren’t many other things….

72
Q

what are the 3 types of non-REM parasomnias?

A
  1. confusional arousals = awakening with confusion
  2. sleepwalking
  3. sleep terrors

in children, NREM parasomnias occur out of stage N3 in the first part of the night while in adults they can occur out of any N1-N3 stage during any part of the night

73
Q

how do you treat non-REM parasomnias?

A
  1. reassurance
  2. BZD if needed

these are benign and don’t cause long term problems and resolve on their own with age

74
Q

A 40-year-old man presents to the office for workup of fatigue. He describes severe daytime sleepiness and may fall asleep while driving. He denies any sudden loss of muscle tone (no cataplexy) or hallucinations before or after falling asleep. He often wakes up feeling tired and his wife complains of his severe snoring. His BMI is 40. What would be the next step:

A. Pulmonary function testing

B. Nocturnal polysomnography

C. Start methylphenidate

D. Start zolpidem

E. Urine free cortisol level

A

B. Nocturnal polysomnography

he has obstructive sleep apnea!

chest goes in and abdomen goes out when he sleeps because of obstruction of the upper airway

75
Q

what is sleep apnea?

A

breathing disruption for at least 10 seconds repeatedly during sleep that is either complete cessation (apnea) or partial (hypopnea) –> sleep disruption –> arousals and less deep sleep –> daytime fatigue/ memory problems

(# of apneas + hypopneas)/hours of sleep = apnea-hypopnea index (AHI)

normal is <5/hour, anything higher is sleep apnea

76
Q

what are the 2 types of sleep apnea?

A
  1. central sleep apnea

2. obstructive sleep apnea

77
Q

what is central sleep apnea?

A

no respiratory effort due to decreased CNS drive

78
Q

what is obstructive sleep apnea?

A

physical airway obstruction due to:
1. decreased pharyngeal muscle tone

  1. thick neck pressing on the upper airways
  2. enlarged tonsils (usually in kids)

more common in men

79
Q

what do you do during a sleep apnea workup?

A
  1. polysomnography
  2. blood-polycythemia due to EPO release from chronic hypoxia
  3. EKG for cardiac arrhythmias
80
Q

what are the symptoms of sleep apnea?

A
  1. chronic fatigue
  2. morning headache
  3. loud snoring (usually for obstructive)
  4. hypertension
81
Q

how do you treat sleep apnea?

A

central sleep apnea is treated with a BPAP to provide mechanical ventilation

obstructive sleep apnea is treated with a CPAP, weight loss or surgical tonsillectomy

82
Q

what are the complications that could result from sleep apnea?

A
  1. arrhythmias
  2. pulmonary hypertension

due to chronic hypoxia stimulating pulmonary vasculature constriction = pulmonary hypertension

83
Q

what is restless leg syndrome?

A 
URGE
U = urge to move
R = rest induced
G = gets better with activity
E = evening/night is worse
84
Q

what causes restless leg syndrome?

A
  1. so it’s a circadian problem and most patients have an underlying iron deficiency so people will have low serum ferritin

iron deficiency can lead to underactive tyrosine hydroxylase and hence low dopamine because TH is the enzyme that makes dopamine – low dopamine means more restless leg syndrome (like parkinson’s tremors)

  1. the other cause of restless leg syndrome is creatine – so pregnant women and people in kidney failure have with high creatine have uremia are at risk for RLS
85
Q

how do you treat restless legs syndrome?

A
  1. dopamine agonists (ropinirole or pramipexole)
  2. gabapentin

anti-convulsive medication that acts on Ca+2 and blocks it which prevents NT release

  1. opioid for severe cases

Neuro Week 6 (8 decks)

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