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EXP NEURO > Neuromodulation > Flashcards

Neuromodulation Flashcards

1
Q

define neuromodulation:

A
  • alteration of nn activity through targeted delivery of stimulus, such as electrical stimulation or chemical agents to specific neurological sites in body
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2
Q

neuromodulation: altered nn activity = altered

A
  • altered communication btw pre/post synaptic neuron
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3
Q

neuromodulation: 2 Qs to ask

A
  • chemical synapse inhibitory/excitatory?

- are we trying to increase/decrease activity at synapse?

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4
Q

neuromodulation: some applications eg.

A
  • essential tremor
  • parkinson’s disease
  • epilepsy
  • depression
  • OCD
  • tourette syndrome
  • obesity
  • angina
  • hypertension
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5
Q

neuromodulation: where can we apply this in nervous sys?

A
  • anywhere

- entire NS operates on converting electrical energy -> chemical signals = all aspects can be neuromodulated

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6
Q

neuromodulation: list (5) ways of modulating

A
  • electrical
  • physical
  • pharmacological
  • genetic
  • optogenetic
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7
Q

ANS regulation of HR: where para preganglionic neurons (2)

A
  • nucleus ambiguous

- dorsal motor nucleus of vagus

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8
Q

ANS regulation of HR: where sym preganglionic neurons (1)

A
  • intermediolateral cell column
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9
Q

ANS regulation of HR: which postganglionic nn for para

A
  • vagus nn
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10
Q

ANS regulation of HR: which postganglionic nn for sym

A
  • inf cardiac nn
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11
Q

ANS regulation of HR: symp features (5) HR, NT, receptor, pre/postganglionic neurons

A
  • increase HR
  • NAd
  • ß adrenoreceptors (atenolol -> bradycardia)
  • postgang: stellate ganglia
  • pregang: arise from SC
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12
Q

ANS regulation of HR: para features (5) HR, NT, receptor, pre/postganglionic neurons

A
  • decreases HR
  • Ach
  • mACh receptors (atropine -> tachycardia)
  • postgang: ‘fat pads’ on heart
  • pregang: arise from brainstem
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13
Q

ANS regulation of BP: MAP =

A

TPR x CO

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14
Q

ANS regulation of BP: major regulator of BP? para/sym NS

A

sym NS

prazosin -> lower BP

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15
Q

ANS regulation of BP: to change CO

A
  • inn heart
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16
Q

ANS regulation of BP: to change TPR

A
  • inn vasculature
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17
Q

ANS regulation of BP: topographical arrangement- upper SC

A
  • blood v in head + neck
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18
Q

ANS regulation of BP: topographical arrangement- lower SC

A
  • blood v in lower limbs
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19
Q

ANS regulation of BP: major resistance vessels? and inn by which NS

A
  • arterioles

- sym NS (å adrenoreceptors)

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20
Q

ANS regulation of BP: baroreceptor reflex features (3)

A
  • reacts to sudden/ongoing changes in BP (keep BP 120/80)
  • increase BP= increase activity of reflex (vice versa)
  • alters BP: simultaneously changing vagal outflow to heart + sym outflow to heart and vasculature
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21
Q

why modulate activity of ANS? 3 answers

A
  1. to understand what function particular nn has
  2. understand pathological changes occur in disease
  3. to correct pathological changes that have occurred
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22
Q

why modulate activity of ANS? 1) how to test function of nn

A
  • using donor heart stimulate vagus - HR slows - remove fluid sample
  • using recipient heart: add fluid to heart = HR also slows
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23
Q

why modulate activity of ANS? 2) elevated HR in CVS related disease may be due to (3)

A
  • increased sym tone
  • reduced para tone
  • BOTH increased sym and reduced para tone
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24
Q

why modulate activity of ANS? 2) pharmacologcially block input to heart, measure change in HR BUT con?

A
  • doesn’t tell u why diff, only acknowledges diff exists
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25
Q

why modulate activity of ANS? 2) nn stimulation controls for? and can determine

A
  • controls for diff in activity of nn

- determines if diff at level of heart (eg. receptor)

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26
Q

why modulate activity of ANS? 2) assumption of NT

A
  • quantal release of NT the same
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27
Q

why modulate activity of ANS? 2) use optogenetics, if no diff to nn stimulation exists?

A
  • diff must be due to diff in nn activity (brain not prod enough/ generating too much nn activity)
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28
Q

why modulate activity of ANS? 3) correct pathological changes characterised by (3)

A
  • reduced vagal tone
  • increased sym nn activity
  • reduced baroreflex function
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29
Q

why modulate activity of ANS? autonomic dysfunctions/pathological changes eg.

A
  • hypertension
  • heart disease
  • arrhythmias
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30
Q

how to restore ANS activity using neuromodulation? correct reduced vagal tone?

A
  • vagal stimulation
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31
Q

how to restore ANS activity using neuromodulation? reduce cardiac sym overactivity?

A
  • stellate ganglionectomy
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32
Q

how to restore ANS activity using neuromodulation? correct reduced vagal tone/sym overactivity? also baroreceptor reflex dysfunction

A
  • baroreceptor activation
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33
Q

how to restore ANS activity using neuromodulation? sym overactivity

A
  • renal denervation
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34
Q

vagus nn: mixed fibre nn types (3)

A
  • afferent fibres
  • somatic motor
  • visceral motor
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35
Q

vagus nn: aff fibres

A

convey info:

  • sensory receptors in upper airways, ear
  • visceral receptors in aortic bodies, aortic arch, thoracic, ab aorta
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36
Q

vagus nn: somatic motor fibres

A
  • inn mm in upper airways
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37
Q

vagus nn: visceral motor fibres

A
  • inn CV, resp and GIT sys
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38
Q

vagus nn: current treatments only target para/sym NS?

A
  • sym NS
39
Q

vagus nn: increasing para activity (eg. exercise, direct vagal stimulation) prevents

A
  • arrhythmias and sudden cardiac death
40
Q

vagus nn: experiment- stimulation of vagus

A
  • increased contralateral vagal input to heart

- reduced contralateral sym input to heart

41
Q

vagus nn: experiment- stimulation also helps (3)

A
  • prevents ventricular fibrillation following myocardial infarction
  • decreases mortality
  • improves L ventricular function in myocardial induced heart failure model
42
Q

vagus nn: experiment- cardiofit sys

A
  • senses HR and stimulates vagus nn exactly 70ms after each atrial contraction
  • make sure HR doesn’t fall too low (55 bpm)
43
Q

phase II feasibility study: study 1 demonstrated?

A
  • safety and efficacy
44
Q

phase II feasibility study: study 2 showed reduction in

A
  • reduced severity of heart failure, increased quality of life
45
Q

INOVATE-HF trial: primary efficacy endpoint

A
  • death or first event triggering worsening of heart failure
46
Q

INOVATE-HF trial: summary vagal nn stimulation

A
  • reduces symptoms of heart failure, improves quality of life BUT not effective in reducing rate of death from any cause/ heart failure events
47
Q

vagus stimulation: possible mechanisms (7)

A
  • decrease HR
  • increase HRV
  • improve baroreflex
  • reduce arrhythmias
  • activation of cholinergic anti-inflammatory pathway
  • cellular changes (NO and cytokines)
  • inhibit RAS
48
Q

vagus stimulation: increase in both aff/eff activity may underlie positive effects observed BUT

A

these changes not sufficient to reduce mortality

  • more studies needed
49
Q

targeting sym input to heart: reducing postgang sym input to heart improves? and results

A
  • improve autonomic control of HR
  • very challenging
  • anaesthetic block of sym ganglia attempted= variable success
50
Q

targeting sym input to heart: cell bodies/axons gives rise to sym nn inn AV node? location?

A
  • cell bodies

- R stellate ganglia

51
Q

targeting sym input to heart: optogenetic stimulation of R stellate ganglion (RSGS) increases/decreases HR

A
  • increases HR
52
Q

targeting sym input to heart: how can optogenetics be used to modulate NS

A
  • excite/ inhibit neurons
  • those that silence cell bodies of nn which give rise to cardiac sym eff -> hypothetically prevent ventricular arrythmias
53
Q

targeting sym input to heart: L stellate ganglion gives rise to inn? and if overactive?

A
  • inn L ventricle

- overactive = ventricular arrhythmias

54
Q

targeting sym input to heart: what is used to ‘measure’ para and sym control of HR?

A
  • HR variability
55
Q

targeting sym input to heart: LF =

A

sym control

56
Q

targeting sym input to heart: HF =

A

para control

57
Q

targeting sym input to heart: LF/HF =

A

sympathovagal balance (questionable though)

58
Q

targeting sym input to heart: optogenetic inhibition of stellate can?

A
  • reduce sym tone

- ‘correct’ sympathovagal balance

59
Q

targeting sym input to heart: optogenetics use stimulates nn more ? than electrical stimulation and can translational capacity now

A
  • more physiological

- need more knowledge of neural circuitry in HR control, utilising techniques in translational capacity

60
Q

baroreceptor: what mimics activation of baro reflex?

A
  • electric stimulation of aortic depressor nn
61
Q

baroreceptor: normal reflex = (2)

A
  • freq dependent decrease of sym nn activity (RSNA)

- HR

62
Q

baroreceptor: normal reflex collectively =

A

decrease BP (MAP)

63
Q

baroreceptor: use modulation of baroreflex to examine how well brain is prod reflex changes in? and eg.

A
  • in BP in disease (kidney disease, LPK)
64
Q

baroreceptor: stimulation of aortic depressor nn understand how changes in CNS cont to ? function in disease

A
  • abnormal baroreflex function
65
Q

baroreceptor: eg. obesity increased/decreased leptin levels causing reduced baroreflex function

A

increased leptin

66
Q

baroreceptor: microinjection of leptin into? will reduce?

A
  • into nucleus solitary tract (baroreceptor aff terminate in CNS) reduce RSNA, HR and BP
67
Q

baroreceptor: define resistant hypertension

A
  • BP >140/90

- despite 3+ antihypertensive meds (incl. diuretic)

68
Q

baroreceptor: resistant hypertension- likelihood of CV event than treatment responsive hypertension

A

3x

69
Q

baroreceptor: what causes/common in people w hypertension

A
  • chronic unloading of baroreceptors

- baroreflex dysfunction

70
Q

baroreceptor: goal for hypertension? baroreceptor stimulation

A
  • decrease sym nn activity, TPR = decrease BP
71
Q

baroreceptor: activation therapy- experiment control and result

A
  • 6 male normotensive dogs
  • electrodes bilaterally around carotid sinus ‘continuous’ baroreflex activation
  • reduced BP, HR, plasma NAd
  • consistent w activation of baroreflex
72
Q

baroreceptor: activation therapy- experiment induced hypertension and result

A
  • fed high fat diet for 6 weeks -> hypertension
  • baroreceptors activated chronically during week 5 of diet
  • reduced BP, HR, plasma NAd which reversed when stopping stimulation
73
Q

baroreceptor: activation therapy- CVRx rheos sys?

A
  • pulse generator (like pacemaker)

- 2 leads wrap around carotid bulbs like hand

74
Q

baroreceptor: device based therapy in hypertension trial? and results

A
  • human patients w resistant hypertension

- reduced SBP 2 yrs

75
Q

baroreceptor: activation therapy (BAT)- rheos pivotal trial experiment

A
  • BAT for first 6 months

- BAT delay initiation for 6 months

76
Q

baroreceptor: activation therapy (BAT)- rheos pivotal trial result

A
  • failed short term efficacy and safety

- 35mmHg reduction of SBP at 12mths

77
Q

renal nn: types of fibres (2)

A
  • both sym eff and

- sensory aff fibres

78
Q

renal nn: increase renal sym activity

A

increased:

  • renal vascular resistance
  • renin release
  • sodium
  • water retention
79
Q

renal nn: excitatory reflexes (aff sensory nn/sym eff?) and increase/decrease sym outflow to other vascular beds

A
  • aff sensory nn

- increase outflow

80
Q

renal nn: nn cont to?

A

resting BP

81
Q

renal nn: renal sym nn activity (RSNA) higher BP = higher/lower sym nn activity?

A
  • higher activity
82
Q

renal nn: increase nn activity = increased/decreased contractility

A
  • increased
83
Q

renal nn: stimulation renal aff nn -> increase/decrease BP through activation of CNS regions of BP

A
  • increase BP
84
Q

renal denervation: surgical sympathectomy increases/decreases BP in malignant hypertension?

A
  • reduces BP
85
Q

renal denervation: hypertension- renal sym nn activity chronically elevated/depressed

A
  • elevated
86
Q

renal denervation: process and correlation of BP reduction =

A
  • surgically/chemically destroying renal nn slows dev hypertension
  • magnitude of BP reduced correlates to kidney NAd content
87
Q

renal denervation: HTN1 test and results?

A
  • BP reduced 1mth sustained 12mths post procedure

- some renal NAd reduced in patients

88
Q

renal denervation: HTN2 test and results?

A

~40% patients in office systolic BP <140mmHg 6mths post

89
Q

renal denervation: HTN3 test and results?

A
  • failed to show clinically sig effect

- 1/3 non responders

90
Q

renal denervation: why went wrong? (3)

A
  • inexperienced interventional cardiologists
  • procedural efficacy
  • rush to get to clinic?
91
Q

neuromodulation: ethical considerations- safety and feasibility (3)

A
  • procedural complications (risk?)
  • long term consequences
  • patient pop
92
Q

neuromodulation: ethical considerations- efficacy (2)

A
  • does procedure really work (eg. renal denervation)

- placebo controls? (ethical consideration too)

93
Q

neuromodulation: ethical considerations- consent (1)

A
  • are patients truly able to consent to procedure
94
Q

neuromodulation: ethical considerations- conflict of interest (1)

A
  • will treating physician benefit? eg. financial gain?

EXP NEURO (10 decks)

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