Feb 5th Flashcards

1
Q

two types of sensitization

A

peripheral and central

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2
Q

central sensitization

A

occurs in the central nervous system, and happens in either the DRG or the spinal cord

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3
Q

peripheral sensitization

A

neurochemical

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4
Q

Skin-nerve preparation

A

take a piece of skin from an animal while it’s still alive, and you tease out a nerve fibre that would have been running from the skin to the DRG and spinal cord and put it in a bath to keep it alive and record from it

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5
Q

what do you look at for skin-nerve preparation

A

number of action potentials per second that the nociceptor has fired

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6
Q

With more bradykinin

A

more action potentials are firing at lower temperatures, including non-noxious temperatures.

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7
Q

Clifford Woolf

A

discovered central sensitization in a sole-authored study published in 1983 in a paper called Nature in which he applied a heat stimulus to rats to measure the lowest amount of mechanical stimulus in grams it would take for the rat to try to withdraw from it

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8
Q

what did Woolf measure his experiment

A

using WDR (second-order) neurons in the spinal cord.

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9
Q

Woolf experiment

A

After the injury, the rats were extremely allodynic for about 5 hours. Before the burn injury, they fire, but it stops really quickly. After the injury, they fire more, and the fire lasts for longer.

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10
Q

what was a surprise in Woolfs experiment

A

the neurons were firing on the contralateral side

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11
Q

only way to explain the transfer of pain from one side to the other was if

A

the WDR neurons themselves had changed such that a stimulus that would normally not be painful before the injury but after the injury, the WDR neurons have changed their properties such that normal stimulation of intact, non-injured skin on the other side of the body is now making them fire as well

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12
Q

Electrophysiological recording can distinguish between

A

peripheral and central sensitization

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13
Q

injuries can cause

A

peripheral and central sensitization

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14
Q

how can you differentiate central and peripheral sensitization

A

Suppose there’s only peripheral sensitization, regardless of where you’re recording from. In that case, you will see a certain amount of firing from before the injury and more firing after the injury, and you will see the same thing in the CNS. If there’s only central sensitization, you wouldn’t see any change in the periphery, but there will be more firing in the spinal cord.

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15
Q

in central sensitization its the __ that has changed

A

the spinal cord neuron

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16
Q

in peripheral sensitization

A

the nociceptor will be activated more

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17
Q

temporal summation or ‘the wind up effect’

A

when you give a pain stimulus in one-second intervals (for example), as the more times you give the stimulus, the more times the neurons will fire.

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18
Q

If stimuli are far enough apart, they will

A

not produce temporal summation and it will simply be a stimulus.

19
Q

if the stimuli are close enough to summate with each other, the pain ratings will

A

get higher and higher the more you give the stimulus

20
Q

Temporal summation is the evidence that

A

central sensitization has occurred

21
Q

Sensitization produces

A

hyperalgesia or allodynia

22
Q

primary vs secondary hyperalgesia

A

Primary hyperalgesia is the thing that happens close to or at the site of the injury. Secondary hyperalgesia is mechanically specific; it doesn’t work with heat stimuli.

23
Q

two types of secondary hyperalgesia

A

bc two types of mechanical stimuli - poking (punctuate and static) vs brushing (stroking and dynamic)

24
Q

By using stroking stimuli, the area of secondary hyperalgesia

A

doesn’t go as far, but it will go further if a punctate stimulus is used.

25
Some evidence of this is 'mirror pain'
where if the injury is on one side of the body, you can see hyperalgesia and allodynia on the other side of the body - and you can apply compounds that either cause analgesia or complete desensitization of the area which gets rid of primary pain, but doesn't do anything to secondary hyperalgesia.
26
secondary hyperalgesia is
mechanically specific; it doesnt work with heat stimuli
27
diagram on L3S54
there's the external stimulus, which is either nothing, an innocuous stimulus (in blue), or a noxious stimulus (in red). The blue is A-beta, and the red is A-delta or a C. The halo symbolizes that the nociceptor is sensitized. The halo is peripheral sensitization. The neurons, or afferents, lead to boxes called the central sensory pathways, which are either the brain or the spinal cord. The box can be blue for normal or red for centrally sensitized.
28
first gray box
if either an innocuous or a noxious stimulus impinges on a nociceptor that is sensitized, even if it is impinging on a normal non-sensitized spinal cord, that will be enough to produce allodynia - in the case of the innocuous stimulus- or hyperalgesia - in the case of the noxious stimulus. However, they will be primary allodynia or hyperalgesia, so you will only find it at the site where the injury is
28
second gray box
there is central sensitization. So, the innocuous stimulus will make a touch fibre fire, and because the spinal cord neuron is sensitized, it will produce allodynia in the secondary area. For hyperalgesia, the same thing occurs, except the stimulus is noxious.
29
third gray box
there is no stimulus at all; this is spontaneous pain caused by the afferents firing by themselves. It is called ectopic firing when afferents fire by themselves, with no peripheral input. If a nociceptor fires ectopic activity, that is spontaneous pain. If a low-threshold neuron or a touch fibre fires ectopic activity, that is paraesthesia. If an A-beta fires ectopic activity and you already have central sensitization, then in addition to spontaneous pain, you will also get dysesthesia.
30
injury produces lots of
plasticity
31
functional plasticity
when whatever is there changes its function to produce sensitization
32
what changes occur in functional plasticity
molecular, synaptic, cellular, and network
33
structural plasticity
when new things are being made or taken away; some physical change has occurred
34
what changes in structural plasticity
can change the number of synaptic spines, the connectivity of the axons (denervation or hypotrophy), and number of cells you have
35
immune cells or glial cells are
very important to the study of pain
36
neuroimmunology happens
both the periphery and spinal cord
37
easy ways to measure pain include
a thermode (a device that you place on the skin that can be heated up), the cold presser test (someone places their hand or arm in cold water), or a pressure algometer (you put it on a particular body part and press down harder and harder until the patient says they feel pain)
38
pain threshold
how much of a specific stimulus (heat, cold, pressure) someone can take until it becomes pain
39
pain tolerance
how much pain stimulus you can take until it becomes too much.
40
problem with pain threshold
it's hard to figure out the exact second that something goes from not being painful to being painful
41
problem with pain tolerance
as a measure is that it can be affected by all sorts of things (someone forcing themselves to hold on for longer than they normally would because of the fact that it's a study, etc.)
42
NRS
numeric rating scale is an 11 point scale, from 0-10