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Integrated Brain > Week 9-10 (Pain and Respiration) > Flashcards

Week 9-10 (Pain and Respiration) Flashcards

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1
Q

<p>What is the definition of pain (2)</p>

A

<p>Unpleasant sensory and emotional experience associated with actual or potential tissue damage</p>

<p>Associated with crying, sympathetic activation, behavioural changes</p>

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2
Q

<p>Why is pain important? (2)</p>

A

<ul> <li>Directs attention to danger and holds attention to it</li> <li>Patients with congenital analgesia (cannot feel phyiscal pain) have reduced lifespan <ul> <li>e.g., biting off tonuges</li> </ul> </li></ul>

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3
Q

<p>What are the fixed factors influencing sensation of pain (4)</p>

A

<p>1. Genetics</p>

<p>2. Age (Older more pain)</p>

<p>3. Sex (Woman more pain)</p>

<p>4. Hair Colour (Redheads have increased sensitivity to thermal pain, and reduced sensitivity to chemical and electrical pain, need more anasthetic)</p>

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4
Q

<p>What are the modifiable factors influencing pain (6)</p>

A

<ul> <li>Context (High adrenaline increases tolerance)</li> <li>Prior life stressors (Early stress modifies later sensitivity)</li> <li>Obesity (Obseity associated with increased sensitvity, might be cormorbid)</li> <li>Anxiety/Depression (Increased sensitivity)</li> <li>Attention (Diverting attention reduces pain sensation)</li> <li>Sleep (Sleep deprivation increases pain sensitvity)</li></ul>

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5
Q

<p>What is the Gate Theory of Pain and what does it explain? (2)</p>

A

<p>Feedback loop in spinal cord to determine which stimuli reaches brain (Chronic stress opens gate; Adrenaline closes gate)</p>

<p>Explains how pain can be ignored on battlefield but intense when upset; Rubbing sore limbs/TENS (distractions) may "close gate"</p>

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6
Q

<p>What is the bioloigcal underpinns of Gate Theory of Pain (2)</p>

A

<ul> <li>Noxious stimulus sensed by smallperiphery nerve fibres and send to spinal cord</li> <li>Distractive stimulus sensed by large periphery nerve fibres and send to inhibitory interneuron and spinal cord. <ul> <li>Inhibitory interneuron reduces pain signal reaching the brain</li> </ul> </li></ul>

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7
Q

<p>What is the pain receptor (3)</p>

A

<p><u>Nociceptors</u></p>

<ul> <li>Sensory receptors capable of transducing noxious stimuli</li> <li>Free neve endings</li> <li>Several class which respond to different stimuli</li></ul>

<p></p>

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8
Q

<p>What are the different stimuli in relation to pain receptors? (5)</p>

A

<p><u>Stimuli</u></p>

<ul> <li>Mechanical <ul> <li>E.g., pressing finger</li> </ul> </li> <li>Temperature(Extreme) <ul> <li>Will remain silent until extreme cold/heat</li> </ul> </li> <li>Electrical <ul> <li>Electrical shock/pain</li> </ul> </li> <li>Chemical <ul> <li>E.g., Capsaicin responds to heat</li> </ul> </li></ul>

<p>> Inflammation: NOinflammation receptor</p>

<ul> <li>Mechanical and increased nociceptor sensitivity</li></ul>

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9
Q

<p>What are the 2 kinds of pain nerves? (3)</p>

A

<ul> <li>Aδ (alpha-delta) fibres <ul> <li>Some myelin, faster for sharp pain; transmit sharp pain</li> </ul> </li> <li>C fibres <ul> <li>No myelin, slower, transmits dull aching pain</li> </ul> </li></ul>

<p></p>

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10
Q

<p>If myelin speeds up speed of trasnmission, and pain is important, why are there so little myelin in the pain nerves? (2)</p>

A

<p>Pain signals are quick due to</p>

<ul> <li>Size of the nerves</li> <li>Number of synapses (few synapses = faster) <ul> <li>From spinal cord to brain has few to no synapses</li> </ul> </li></ul>

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11
Q

<p>Where is the synapse in the spinal cord? What does it release?</p>

A

<p>Pain signals synapse in the <u>substantia gelantinosa</u> in the<u> dorsal horn</u> of the spinal cord, releasing...</p>

<ul> <li>Glutamate</li> <li>Substance P <ul> <li>Small pain = Glutamate</li> <li>Large pain = Glutamate + P</li> </ul> </li></ul>

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12
Q

<p>What are the two sense pathways? (3 ea.)</p>

A

<p><u>Touch</u>: Mechanoreceptors</p>

<ul> <li>At ipsilateral side at spinal cord</li> <li>Transverse to contralateral side at medella</li> <li>To thalamus and to contralateral somatosensory cortex</li></ul>

<p><u>Pain:</u>Nocireceptors</p>

<ul> <li>Transverse to contralateral side at spinal cord</li> <li>At contralateral side at medella</li> <li>To thalamus and to contralateral somatosensory cortex</li></ul>

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13
Q

<p>What are the ascending pain pathways, i.e. where are the places pain signals terminate? (3)</p>

A

<ul> <li>Primary somatosensory cortex (Where)</li> <li>Anterior Cingulate (Sense of pleasantness) <ul> <li>Emotional aspects</li> <li>Sympathetic pain</li> <li>Social rejection (not the same as pain sensation)</li> </ul> </li> <li>Insular (Also has somatosensory distrbution) <ul> <li>Modulate physical pain response</li> </ul> </li></ul>

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14
Q

<p>What are the descending pain pathways, i.e. which brain areas modulatespain? (2)</p>

A

<p>Amygdala and Hypothalamus modify pain responses by activating periaqueductual gray (PAG)</p>

<p>PAG usesendorphins/endogenous morphine, inhibiting pain signals (Endorpins bind to opiate receptor in PAG)</p>

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15
Q

<p>How does the brain deal with prolonged pain? (1)? What else cause endorphin release? (1)</p>

A

<p>Since it is unnecessary, brain dimishes prolonged pain through endorphin release, which binds to opiate receptors in PAG</p>

<p>Inescapable pain, exercise, sex leads to increased endorphin release and reduced pain sensitivity</p>

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16
Q

<p>What are some 4drug treatments for pain?</p>

A

<p>1. Opiates</p>

<p>2. Panadol/Tylenol</p>

<p>3. Placebo</p>

<p>4. Acupuncture</p>

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17
Q

<p>Drug treatment #1: Opiates (2)</p>

A

<p>Blocks release of substance P in PAG</p>

<p>Same mechanism as endorphines</p>

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18
Q

<p>Drug treatment #2: Panadol/Tylenol (3)</p>

A

<ul> <li>Exact mechanisms of analgesia unkown.</li> <li>Inhibits synthesis of prostaglandins (pro-inflammatory)</li> <li>Analgesia is presumed central and related to reduced serotonin, opioids or through the endogenous cannabinoid system as blocking these systems reduce the analgesic effect.</li></ul>

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19
Q

<p>Drug treatment #3: Placebo (2)</p>

A

<ul> <li>Quite effective</li> <li>Reduce emotional aspects of pain via. reduced activity in cingulate cortex (not somatosensory)</li> <li>Increased release of endorphins (Placebo + Naxolene < Placebo due to placebo effect)</li></ul>

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20
Q

<p>Drug treatment #4: Acupuncture</p>

A

<p>Acupuncture releases endogenous opioids</p>

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21
Q

<p>Evidence that social exclusion hurts?</p>

A

<ul> <li>ACC activation in virtual ball game. <ul> <li>Activation correlated to extent one felt excluded</li> </ul> </li></ul>

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22
Q

<p>Evidence of heartbreak and pain</p>

A

<p>Recount recent unwanted breakup while viewing ex's picture<strong>vs</strong>painful stimulus</p>

<ul> <li>Same brain regions in both conditions (ACC, Insula, Somatosensory)</li> <li>Similar findings in bereaved indiviuals</li></ul>

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23
Q

<p>Evidence ofTylenol for social pain (3)</p>

A

<ul> <li>Tylenol participants had reduced daily hurt feelings over time (vs placebo didn’t change)</li> <li>Tylenol had low activation of ACC &amp; insula after virtual ball game</li></ul>

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24
Q

<p>Evidence of love and pain?</p>

A

<ul> <li>Painful stimuli in 7 conditons</li> <li>Holding their partner’s pic/hand = Reduced pain ratings</li> <li>Holding a stranger’s hand / ball = No improvement in pain ratings</li></ul>

<p>Note: 44% reduction in pain rating when viewing a picture of their partner compared to holding hand</p>

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25
Q

<p>Evidence that hyponsis alters pain?</p>

A

<p><u>Methods</u></p>

<p>Arms in ice water. Hypnosis vs no hypnosis</p>

<p><u>Results</u></p>

<ul> <li>Hypnotised group rated pain just as intense but less unpleasant</li> <li>Hypnosis alters activity in: ACC, Amygdala, Thamalus, Insula, Somatosesnsory cortex (Same areas)</li></ul>

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26
Q

<p>Define Chronic Pain (4)</p>

A

<ul> <li>Pain that outlasts expected healing time (3-6mo)</li> <li>Generally not due to residual injury/inflammation <ul> <li>Poor correlation with signs of injury and pain (20-25% osteoarthrities patients who have knee replcement don't get improvement in pain)</li> </ul> </li> <li>Prevalance is about 10-50%, depending on type of pain</li> <li> <p>Increased pain sensitvity is a good indicator of future chronic pain</p> </li></ul>

<p></p>

<p></p>

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27
Q

<p>What are predisposing factors to Chronic Pain? (5)</p>

A

<ul> <li>Women <ul> <li>1.5-2x higher pain sensitivity and double rate of chronic pain</li> </ul> </li> <li>Early life pain/stress and prior injury <ul> <li>Increase adult pain sensitivty/persistent pain</li> </ul> </li> <li>Stress <ul> <li>Rat pups separated from mum have pain signs</li> </ul> </li> <li>Psychological/Personality factor <ul> <li>Fear of pain, catastrophising</li> </ul> </li> <li>Depression/Anxiety <ul> <li>Reciprocal</li> </ul> </li></ul>

<p></p>

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28
Q

<p>What is the pathophysiology of chronic pain. (4)</p>

A

<p>Due to neuroplasticity both peripherally and centrally</p>

<ul> <li>Peripheral changes in multiple receptors</li> <li>Neurons grow and increase synaptic connections to second order neurons in medulla</li> <li>Gilal cellsinspinal cord remodel to intensify pain trasmission (e.g., produce substance P)</li> <li>CNS changes resulting in central sensitisation <ul> <li>Pain signals without pain stimulus</li> <li>Lower pain threshold</li> </ul> </li></ul>

<p>Pain becomes a disease itself</p>

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29
Q

<p>What is the link between depression and chronic pain? (3)</p>

A

<ul> <li>Bidirectional (65% depression have chronic pain;50% chronic pain have depression;Longitudinal studies depressive symptoms predict future pain)</li> <li>Comorbid patients have: <ul> <li>More intense pain</li> <li>Greater disability from pain</li> <li>Poorer response to pain treatment</li> </ul> </li> <li>Treating depression improves pain treatment</li></ul>

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30
Q

<p>Psychological Interactions of Depression vs Normal in Chronic Pain</p>

A

<p><u>Psychological Interactions</u></p>

<p>Injury > Pain experience</p>

<p>Depression:</p>

<ul> <li>Pain <strong>catastrophizing</strong> > Fear > ... > Pain experence</li></ul>

<p>Normal:</p>

<ul> <li>No Fear > Confrontation > Recovery</li></ul>

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31
Q

<p>What is the relationship between meditation and pain?</p>

A

<p>Pain reduced following mindfulness meditaiton</p>

<ul> <li>Reduced pain-related activation of somatosensory cortex and insula</li> <li>Increased activation of ACC (Contrary to expectation)</li> <li>Reduced amygdala activation andnegative emotions in responseto pain</li> <li>NOT DUE TO ENDORPHINS <ul> </ul> </li></ul>

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32
Q

<p>What is the link between sleep and pain? (2)</p>

A

<ul> <li>High comorbidity: 55-88%</li> <li>Bidirectional <ul> <li>Sleep disruption and insomnia increases risk of chronic pain</li> <li>Pain inhibits sleep</li> </ul> </li></ul>

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33
Q

<p>What is the neurological explanation regarding sleep and chronic pain (1+4)</p>

A

<p>Reduced SWS and REM causes <strong>hyperalgesia</strong> (stimulus that should not be painful is painful) whereas warmth dedection and other tactile stimuli are unchanged</p>

<ul> <li>Reducing descending pain inhibitory pathway</li> <li>Increasing Inflamamatory cytokines</li> <li>Reduces inhibition from distraction</li> <li>Modified central sensitization</li></ul>

34
Q

<p>Mechanism 1: Descending pain inhibitory pathway.</p>

<p>Methods and Results</p>

A

<p><u>Methods:</u>Conditioned pain modulation</p>

<ul> <li>Quantify force required before pain (<em>baseline threshold)</em></li> <li>Exposure to ice cold bath (Prolonged pain releases endorphins in PAG)</li> <li>Increase pain threshold to a secondary stimulus</li></ul>

<p><u>Results</u></p>

<ul> <li>Ice bath does not increase pain threshold after sleep disruption> Reduce effectiveness of pain inhibitory pathway</li> <li>Sleep disruption affects pathway more than deprivation</li></ul>

35
Q

<p>Mechanism 2-4: Attention regulation and sleep.</p>

<p>Elaborate: Methods and Results</p>

A

<p>Sleep loss impairs neurocognitive function, maybe distraction is poor when tired</p>

<p><u>Methods</u></p>

<ul> <li>Pain v.s. Pain + Video Game</li> <li>Measured pain, redness (inflammation), sensation alteration (central sensitisation)</li></ul>

<p><u>Results</u></p>

<ul> <li>Distraction reduced pain rating in well-slept indiviudals</li> <li>More redness and larger zone of altered sensation in low sleep group, indicating inflammatory and spinal modification</li></ul>

36
Q

<p>What is fibromyalgia? What are some symptoms (4)?</p>

A

<p><u>Fibromyalgia</u></p>

<ul> <li>Chronic widespread pain</li> <li>2% prevalance</li></ul>

<p><u>Symptoms</u></p>

<ul> <li>Unrefreshing sleep &amp; fatigue</li> <li>Cognitive impairment, lifetime depression</li> <li>GI symptoms</li> <li>Allodynia (non-painful stimulus becomes painful)</li></ul>

<p></p>

37
Q

<p>Reasons behind Fibromyalgia? (3)</p>

A

<p>1. Central proessing of pain is altered (Heightened sensation)</p>

<ul> <li>Lowered pressure pain threshold</li> <li>Increased somatosensory activation for any level of pressure</li></ul>

<p>2. Ascending pathways abnormal</p>

<ul> <li>Increasing CSF substance P and nerve growth factor</li></ul>

<p>3. Descending pathways abnormal</p>

<ul> <li>Increased CSF serotonin and norepinepherine (which binds to opiatereceptors)</li> <li>Reduced ACC activity</li></ul>

38
Q

<p>What is the link between sleep and fibromyalgia? What does PSG show? (3)</p>

A

<ul> <li>No insomnia</li> <li>Restless or light sleep with frequent awakening <ul> <li>Reduced SWS and spindlesalong with <strong>alpha intrusions</strong> (key)</li> <li>Alpha intrudes into delta sleep</li> </ul> </li> <li>Poor sleep associated with worsening of symptoms</li></ul>

39
Q

<p>What is the correlation with fibromyalgia and sleep?</p>

<p></p>

A

<p>Correlation:</p>

<ul> <li>Poor sleep quality prediced Fibromyalgia development</li> <li>Non-restorative sleep strongest predictor of widespread pain</li></ul>

<p></p>

40
Q

<p>If we improve sleep, can we improve fibromyalgia?</p>

A

<p>Treatment:</p>

<ul> <li>Sodium oxybate <ul> <li>Yes for pain, sleep, fatigue, life quality</li> </ul> </li> <li>CBTi <ul> <li>Yes for sleep, fatigue, daily functioning, pain catastrophising</li> <li>No for pain</li> </ul> </li></ul>

<p>Best way to reduce chronic pain is to reduce acute pain</p>

41
Q

<p>Why study respiration (3)?</p>

A

<ul> <li>Essential for life: Provides O2 and removes CO2 to ensure correct cellular functioning (gas exchange).</li> <li>Basis for multiple critical behaviours: speaking, olfaction, emesis</li> <li>Strong links to emotional centres in brain</li></ul>

42
Q

<p>How gas exchange occurs? (3)</p>

A

<p><u>Inspiration</u></p>

<ul> <li>Fresh air enters the lungs during inspiration</li> <li>(Low O2;high CO2)blood entering the lungs from the body has the O2 replenished and CO2 removed by diffusion in the alveoli.</li></ul>

<p><u>Expiration</u></p>

<ul> <li>High CO2/low O2 air is breathed out</li></ul>

43
Q

<p>What is the anatomy of the respiratory system? (4)</p>

A

<ul> <li>Air gets split up and divided 24 times</li> <li>24th level: <strong>terminal bronchiole</strong>, and the end is the <strong>Alveolus</strong></li> <li><strong>Alveolus</strong>is a thinned-walled structure whichair can enter</li> <li>Capillary surroundingalveolus allows simple diffusion, whereLow O2&amp; high CO2 blood entering the lungs from the body has the O2 replenished and CO2removed</li></ul>

44
Q

<p>What are the respiratory muscles for inspiration and explain how it works? (2+3)</p>

A

<ul> <li>Active</li> <li>Diaphragm and Intercoastal Muscle (Muscle in-between ribs) <ul> <li>Diaphragm contracts and pulls down</li> <li>Intercostal muscle contract and pull ribcage upwards and outwards</li> <li>Thorax volume increases, creating negative pressure in thorax and air flows in</li> </ul> </li></ul>

45
Q

<p>What are the respiratory muscles for expirationand explain how it works.</p>

A

<ul> <li>Passive at rest, relyingon recoil of the lungs</li> <li>Muscles (diapgram &amp; intercostal) relax, diagragm returning to rest position creates positive pressure in throax, where air flows out</li> <li>Active during exercise/stress using abdonimal muslces, rapidly constricting thorax and pushing air out</li></ul>

46
Q

<p>Neural innervation of respiration (3)</p>

A

<ul> <li><strong>Phrenic nerves</strong>innervate <u>diaphragm</u>. Originates from<strong>cervical spinal cord (C3-C5)</strong>,</li> <li><strong>Intercostal nerves</strong>innervaes <u>intercoastal muscles</u>. Originates from<strong>thoracic spinal cord (T1-T11)</strong></li> <li>Nerves originating from <strong>lumbar spinal cord</strong> innervates <u>accessory muscles </u>(e.g., abdomen; activated during high work/cough)</li></ul>

47
Q

<p>Main regions for control of respiratory system (4)</p>

A

<ul> <li>Pre Botzinger Complex</li> <li>DRG and VRG part of pre-botzinger and botzinger</li> <li>Retrotrapezoid Nucleus (RTN)</li> <li>Pontine respiratory group (PRG)</li></ul>

<p></p>

48
Q

<p>Function of Respiratory Control Region #1</p>

A

<p>Pre Botzinger Complex</p>

<ul> <li>Main respiratory generator (pacemaker neurons of respiratory control)</li> <li>Innervates intercostal muscles</li></ul>

49
Q

<p>Function of Respiratory Control Region#2</p>

A

<p>DRG and VRG</p>

<ul> <li>DRG Innervates the diaphragm <ul> <li>Signal from Pre Boetzinger complex passes toDRG before diaphragm</li> </ul> </li> <li>VRG Inntervates abdominal muscles and intercoastal muscles <ul> <li>Direct connection</li> </ul> </li></ul>

50
Q

<p>Function of Respiratory Control Region #3</p>

A

<p>RTN</p>

<ul> <li>Detects CO2 buildup in body and responds to it by increasing breathing rate (to maintain homeostasis)</li> <li>O2 and CO2 levels are also sensed in the peripheral arteriesand these peripheral signals are sent to the RTN via nerves.</li> <li>Sends info to brain</li></ul>

51
Q

<p>Function of Respiratory Control Region #4</p>

A

<p>Pontine respiratory group (PRG)</p>

<ul> <li>Voluntary control of breathing</li></ul>

52
Q

<p>What are some peripheral inputs (bottom-up)to the respiratory centers (2)</p>

A

<ul> <li>Chemosensors <ul> <li>Through RTN (RTN responds to CO2)</li> </ul> </li> <li>Lung irritant and stretch <ul> <li>Through DRG (part of pre boitzinger complex)</li> </ul> </li></ul>

53
Q

<p>What arecentral inputs to the respiratory centers</p>

A

<p>Top-down primarily via. PRG (voluntary inputs)</p>

<ul> <li>Volitional, Pain, Temperature, Emotion</li> <li>Speech, Swallow, Cough, Sneeze, Hiccup</li> <li>Sleep (-), Exercise (+), Defecation, Parturition</li> <li>Panting, sonar (animals)</li></ul>

<p>All of these inputs from other brain regions, come in via the PRG and this is how all the signals modulate breathing pattern and are integrated into the control of our breathing</p>

54
Q

<p>What is the amygdala's association with respiratory control? (3)</p>

A

<ul> <li>Amygdala–PRGconnection <ul> <li>Emotional stimuli increases respiratory rate</li> </ul> </li> <li>Amygdala–DRG connection <ul> <li>Inspired volume (and cardiovascular) increase</li> <li>Fear/anger: increase respiratory rate and sometimes depth</li> <li>Positive affect: slow and deep (excited) or shallow (calm)</li> </ul> </li> <li>Bi-directional links: Basolateral amygdala (and hypothalamus) are also CO2 sensitive.</li></ul>

55
Q

<p>What is panic disorder? (3)</p>

A

<ul> <li>Frequent and unexpected acute panic attacks</li> <li>Panic attack is anepisode (about 30min) of overwhelming anxiety and distress with air hunger, shortness of breath, hyperventilation</li> <li>Hyperventilation leads to low CO2,causing many symptoms</li></ul>

<p></p>

56
Q

<p>Why does panic disorder occur? (4)</p>

A

<ul> <li>Suffocation “false alarm” hypothesis (Stress > Breathe out too much > Lower CO2> Symptoms > More Stress)</li> <li>Heightened responsiveness to CO2</li> <li>Increased sigh frequency</li> <li>Increased central apnea in sleep</li></ul>

57
Q

<p>Why are paper bags effective in hyperventilation? (2)</p>

A

<ul> <li>Paper bag reduces hypocapnia (state of reduced CO2), which means increases CO2</li> <li>Rebreathing their own air: Bag has higher CO2concentration, breath in more concentrated CO<span>2<span>air,</span></span>normalise CO2levels</li></ul>

58
Q

<p>What are breath holding spells and why? (3)</p>

A

<ul> <li>Involuntary breath holding in toddlers when upset, leading them to turn blue, pass out, and have a seizure</li> <li>Emotional input to the respiratory controller is very strong! (Overwhelms respiratory system)</li> <li>Prevalence ~ 5% of toddlers.</li></ul>

59
Q

<p>What is the link between dyspnea and mood</p>

A

<ul> <li>Dyspnea is a term for the discomfort associated with being short of breath/breathless (e.g., extreme exercise)</li> <li> <p>Did intense exercise whilst viewing images: Negative images had greater dyspnea intensity and bothersomeness than positive images.</p> </li></ul>

60
Q

<p>What is the link betweendeep breathing and stress</p>

A

<ul> <li>Relaxing increases parasympathetic activity, reducingcortisol</li> <li>Relaxing vs Attentive deep slow breathing on pain threshold, autonomic activity, mood <ul> <li>Relaxed deep breathing: Pain threshold increased and sympathetic activity decreased</li> <li>Both relax/attentive deep breathing: Mood incerase</li> </ul> </li></ul>

<p></p>

61
Q

<p>What is Sleep Apnea?</p>

A

<ul> <li>Condition characterised by absent or greatly reduced breathing during sleep (O2 falls, CO2 rises)</li></ul>

<p><u>Definitions</u></p>

<ul> <li>Apnea: Termination of airflow for >10s</li> <li>Hypopnea: >50% decrement in airflow for >10s associated with either: an arousal from sleep or a >3% fall in arterial oxygen saturation (Hypopnea must have a consequence)</li></ul>

62
Q

<p>What is the Apnea/Hypopnea Index (AHI)</p>

A

<p>Feuqency of apnea/hypoapnea eventsper hour</p>

<p>Normal: AHI <5 </p>

<p>Mild: AHI = 5-15 + Sleepiness</p>

<p>Moderate: AHI = 15-30 </p>

<p>Severe: AHI >30</p>

63
Q

<p>What iscentral vs obstructive sleep apnea? (2)</p>

A

<p>Central:</p>

<ul> <li>Won’t breathe</li> <li>No respiratory efforts during sleep</li></ul>

<p>Obstructive:</p>

<ul> <li>can’t breathe</li> <li>Respiratory efforts but no breathing during sleep</li></ul>

64
Q

<p>What is the prevalance of central sleep apnea?</p>

A

<p>1%.However, it is common in some conditions</p>

<ul> <li>Congestive heart failure (CHF)</li> <li>Congenital Central Hypoventilation Syndrome (CCHS)</li> <li>Opioids</li></ul>

<p></p>

65
Q

<p>What is Congestive Heart Failure (CHF)</p>

A

<ul> <li>Damaged heart <strong>delays</strong> the feedback of blood O2/CO2 to the brain</li> <li>No breathing > Hyper ventilation > No breathing</li></ul>

66
Q

<p>What isCongenital Central Hypoventilation Syndrome (CCHS)</p>

A

<p>Genetic condition of abnormal RTNfunction such that patients do not respond to CO2.</p>

<p>(RTN detects CO2levels)</p>

67
Q

<p>What is opiods (how it relates to apnea)? (2)</p>

A

<ul> <li>Reduce the responsiveness to low O2 and high CO2 (RTN and peripheral chemoreceptors)</li> <li>Inhibit the Pre-Boetzinger neurons</li></ul>

<p>(Pre-Boetzinger = Pacemaker)</p>

68
Q

<p>Consequences of CHF, CCHS, Opiods</p>

A

<p>CHF: Sleepiness, disturbed sleep (<strong>no mortality</strong>)</p>

<p>CCHS: death or serious brain damage</p>

<p>Opioids: death (accidental overdose).</p>

69
Q

<p>Treatments of CHF, CCHS, Opiods</p>

A

<p>CHF: optimise heart function, artificial ventilation.</p>

<p>CCHS: artificial ventilation.</p>

<p>Opioids: reduce opioids, artificial ventilation</p>

70
Q

<p>What isObstructive Sleep Apnea (2)</p>

A

<p>A prevalent disorder of repetitive upper airway collapse during sleep (airway is blocked)</p>

<p>Breathing efforts continue during sleep.</p>

71
Q

<p>Hypnogram of OSA</p>

A

<p>People with OSAhave reduced SWS and REM, oxygen saturation, and increased arousal</p>

72
Q

<p>Biological cause of OSA</p>

A

<p>Many muscles surround the upper airway that stiffen and dilate it. OSA patients have smaller upper airways</p>

<ul> <li>During wake, these muscles have high activity which holds the airway open in OSA.</li> <li>At sleep onset this “neuromuscular compensation” is lost, resulting in upper airway collapse.</li> <li>As sleep persists (SWS/Stage 2), muscle activity increases often to levels above those in wake, this can sometimes result in stable breathing.</li> <li>In REM, muscle atonia leds to collapse of airway</li></ul>

73
Q

<p>What is an upper airway dilator muscle</p>

A

<p>The genioglossus (GG, tongue) is the largest, most extensively studied muscle.</p>

74
Q

<p>Results from neuromuscular compensation study on OSA patients.</p>

A

<p>OSA</p>

<p>- Higher activiation of muscle during wake (compensatory), but when they enter sleep, they have a greater drop-off (less compensatory mechanism)</p>

<p>- In N2/SWS, the muscle activation jumps back to wakefulness levels</p>

75
Q

<p>In single motor unit EMG on tongue muscles, what were the findings on OSA patients?</p>

A

<p>In sleep onset, If 1/2 neurons falls while the others maintain constant = Sleep and Respiratoryinfluence independently</p>

<p>In sleep onset, if all neurons fall: Sleep influences Respiratory</p>

<ul> <li>Single-motor unit EMG suggest sleep and respiratory have independent inputson HG muscle</li></ul>

76
Q

<p>Pathophysiology of OSA</p>

A

<p>Fall Asleep > (Dilator muscle activity fall) > Obstruction</p>

<p>> [Respriatory Drive Increase (Increased CO2; Decreased O2)] > Arousal</p>

<p>> (Dialtor muscle activity returns) > Airway open > (Hyperventilation) > Fall Asleep</p>

77
Q

<p>Consequences of OSA. Why?</p>

A

<ul> <li>Behavioural</li> <li>Neurocognitive</li> <li>Cardiovascular</li> <li>Metabolic</li></ul>

<p>Thought to be due to the repetitive</p>

<p>- Arousal (disrupted/fragmented sleep)</p>

<p>- Low oxygen levels (hypoxia)</p>

78
Q

<p>What is the first symptom of OSA (3)</p>

A

<p><u>Excessive Daytime Sleepiness (EDS)</u></p>

<ul> <li>Subjective and objective signs of sleepiness in OSA</li> <li>Typically more severe sleepiness with more severe OSA.</li> <li>But there is great variability between individuals</li></ul>

79
Q

<p>What is the second symptom of OSA (2)</p>

A

<p><u>Mood and behavioural disorders</u></p>

<p></p>

<ul> <li>Patients are often irritable, impatient and moody. <ul> <li>~40% of OSA patients have depressive symptoms.</li> <li>OSA is a risk factor for developing depression in longitudinal studies</li> </ul> </li> <li>Anxiety and PTSD also more common in OSA</li></ul>

80
Q

<p>What is the neurocognitive consequneces of OSA</p>

A

<p><u>Attention/Vigilance</u></p>

<p>- Impaired in dose dependent fashion (individual variability present)</p>

<p>- May lead to other deficits</p>

<p>Memory and learning not examinable</p>

<p></p>

81
Q

<p>Neurocognitive vulnerability in OSA patients: Experiment</p>

A

<ul> <li>OSA and normal patients did well in beginning of driving test</li> <li>But in 4 hours of sleep, OSA patients did worse than control (comparable to alcohol)</li></ul>

82
Q

<p>Treatments for OSA</p>

A

<p>1.Continuous Positive Airway Pressure (CPAP)</p>

<p>- Reverse vacuum cleaner attached to a mask to physicall force aiway open. However, it is uncomfortable and only 1/2 of the patients will wear it</p>

<p>2.Mandibular Advancement Splints (MAS)</p>

<p>- Enlarge airway by pulling jaw open. 50% success rate</p>

<p>3.Airway Surgery</p>

<p>- Enlarge airway. 50% success rate.</p>

<p></p>

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