Pain and Temperature Sensations Flashcards

1
Q

Core Body Temperature

A

37⁰ C

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2
Q

Body temperature has a

circadian fluctuation of

A
  1. 5-

0. 7°C (1-1.5° F)

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3
Q

Temperature is lowest at

—, highest in the —

A

6:00am

evening

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4
Q

Temperature regulation is less

precise in

A

young children;
normally have a temperature
that is 0.5°C or so above adults.

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5
Q

Thermal Receptors (thermoreceptors) are on

A

free nerve endings
& commonly found in the skin. Also in hypothalamus, spinal cord,
& deep tissues.

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6
Q

Categorized by their different sensitivities: (2)

A

cool

warm

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7
Q

Cool and warm receptors innervate

A

discrete regions of skin

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8
Q

There are – times as many cool receptors at any skin surface

A

3-10

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9
Q

— are activated by extreme cold or heat

A

Nociceptors

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10
Q
Which do you 
perceive first-   
a thermal or 
mechanical 
sensation?
A

mechanical

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11
Q

After thermoreceptors are activated,
Warm signals are transmitted by:
Cool signals are transmitted by:

A

C and Aδ fibers

Aδ and C fibers

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12
Q

The mechanism of thermal sensation is most likely achieved by
sensing a change in

A

metabolic rate

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13
Q

— increases the rate of intracellular chemical

reactions

A

Temperature

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14
Q

Several Transient Receptor Potential (TRP) channels

have been identified, each sensitive to a different

A

temperature range. Some chemicals (Capsaicin, Menthol)

elicit thermal sensations, too.

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15
Q

Temperature Perception

Based on the Activation of a

A

Combination of the Receptors

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16
Q

COLD PAIN: (5)

A
Tickling, 
Pricking, 
Aching, 
Burning, 
Numbing
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17
Q

HOT PAIN: (5)

A
Sharp, 
Pricking, 
Stinging, 
Burning, 
Throbbing
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18
Q

If skin reaches —, cold/pain fibers are no longer stimulated.

A

freezing

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19
Q

At ~ –°C, heat/pain fibers are activated.

Sometimes cold fibers are activated, too—

A

45

paradoxical cold

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20
Q

Average skin

temperature =

A

34-35ºC;
equal activation of cool
and warm receptors.

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21
Q
Adaptation of Thermoreceptors
• They mostly (but never completely) 
adapt to --- ---; BUT 
they quickly change their activity in 
response to ---
A

constant temperature
changes in temperature.
They are very sensitive to changes
in temperature.

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22
Q

Adaptation of Thermoreceptors
• If the temperature reaches one of the
pain thresholds, the sensation
becomes

A

more persistent throughout

the stimulus

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23
Q

Sensitivity of Thermoreceptors
• Warm and Cool receptors are best able to detect a change at the
— of their temperature sensitivity (that is where they are
most sensitive)

A

mid-range

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24
Q

Sensitivity of Thermoreceptors
• If nociceptors are simultaneously activated, the system is even
better able to

A

discern small changes in temperature

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25
Q

As temperature increases (or decreases) within a range of a thermoreceptor’s sensitivity,

A

more and more receptors are activated, based on their varying thresholds. Thus perception is increased.

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26
Q

There is also an increase in the rate that — receptors fire (but not nociceptors)

A

thermal

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27
Q

The greater the area of skin affected by a thermal stimulus, the greater the

A

number of receptors, receptive fields, and first order neurons activated and thus the greater the perceived sensation.

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28
Q

There is a much greater ability for detection of a — stimulus if a large region is activated.

A

temperature

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29
Q

Receptors are primarily sensitive to —, but certain

receptors are also sensitive to —

A

temperature

chemicals

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30
Q

Vanilloid Receptor Subtype (3)

A
  1. TRPV1 Receptor
  2. Activated by capsaicin, temperature >43°C, and protons
  3. Decreases the threshold of channel activation so that
    heat is perceived at 33°C.
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31
Q

Cold-Menthol Receptor Type I (CMR1/TRPM8) (2)

A
  1. Menthol and related compounds
  2. Decreases the threshold of the channels so that warmer
    compounds are perceived as cold.
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32
Q

Characteristics of Thermoreceptors in Orofacial Region

receptive field size:

A

Small receptive fields (nociceptive thermal receptors

have large receptive fields)

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33
Q

Characteristics of Thermoreceptors in Orofacial Region

warm vs cool

A

More cool than warm receptors
BUT, whole mouth studies indicate that subjects are
better able to accurately detect increments of
warming rather than cooling

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34
Q

Characteristics of Thermoreceptors in Orofacial Region

the face vs inner mucosa

A

The face is 2-4 times as sensitive to thermal change

(warming) as the inner mucosa

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35
Q

Characteristics of Thermoreceptors in Orofacial Region
Thermoreceptors in — are the most sensitive to
changes in temperature.

A

tongue

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36
Q

Due to activation of nociceptors. This usually results in the
perception of

A

PAIN, an unpleasant & emotional experience

associated with actual or potential tissue damage.

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37
Q

nociception and pain relationship

A

All nociception produces pain, though not all pain

results from nociception.

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38
Q

Unlike most sensory modalities, pain can be evoked

by

A
any stimuli (mechanical, thermal or chemical) if it 
is strong enough.
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39
Q

We sense pain so that the body can (3)

A

detect, localize, and limit tissue damage.

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40
Q

PAIN, whatever its cause, is never —. Pain is the

most common reason patients (2)

A

benign

seek healthcare AND the most common symptom of disease.

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41
Q

types of acute pain (2)

A

somatic

visceral

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42
Q

acute pain

A

Physiologic Pain; <6 months duration

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43
Q

Somatic:

A

From skin, subcutanous tissues or mucus
membranes (Superficial) or muscles, tendons, joints or
bones (Deep).
– Superficial Somatic: localized, sharp, pricking and burning
– Deep Somatic: dull, aching, diffuse and can be referred

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44
Q

Visceral:

A

Due to a disease process or abnormal function
involving an internal organ (Visceral) or its covering
(Parietal).
– True Visceral: dull, diffuse, poorly localized and associated with
nausea and autonomic symptoms.
– Parietal Visceral: sharp, stabbing and better localized than true
pain.

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45
Q

Both types of visceral pain can be –

A

referred

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46
Q

Referred pain most frequently occurs with pain of

— Origin

A

visceral (& sometimes parietal)

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47
Q

Two nociceptive afferent neurons—from different regions of the
body—converge on the same second order neuron. The brain
doesn’t know which is the true source of input and may

A

make a

mistake in interpretation.

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48
Q

chronic pain

A

Pathologic Pain; occurs beyond the usual course of an acute

disease or after a reasonable time for healing to occur

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49
Q

3 types of chronic pain

A

nociceptive
neuropathic
mixed pain

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50
Q

Nociceptive:

A

Due to activation of nociceptors

51
Q

Neuropathic:

A

Due to neuronal injury
• Pain is paroxysmal, sharp and stabbing
• Pain is associated with Hyperalgesia (increased
sensitivity to pain)

“Neuropathic pain includes pain associated with diabetic neuropathy,
causalgia, phantom limbs, postherpetic neuralgia, stroke, spinal cord injury,
and multiple sclerosis. Cancer pain and chronic low back pain may have
prominent neuropathic components.”

52
Q

Mixed Pain

A

combo of nociceptive and neuropathic

53
Q

autonomic responses are only a part of — pain

A

acute

54
Q

Moderate to severe pain can
affect function of every
organ AND adversely
influence postoperative (2)

A

morbidity & mortality.
Poor pain control will
worsen patient outcomes!

55
Q

Nociceptors are usually found on free nerve endings and

are sensitive to: (3)

A
  1. Mechanical Stimuli
  2. Thermal Stimuli
  3. Chemical Stimuli
56
Q

Chemicals known to excite nociceptors: (9)

A
Substance P, 
ATP, 
calcitonin gene related peptide (CGRP), 
glutamate, 
aspartate, 
Bradykinin, 
potassium, 
Histamine, 
serotonin
57
Q

Chemicals known to sensitize nociceptors: (4)

A

Substance P,
Prostaglandins,
Histamine,
Bradykinin

58
Q

Chemicals known to inhibit nociceptors: (3)

A

Enkephalins,
β Endorphin,
Cannabinoids

59
Q

Summation of

nociception is —

A

spatial
(based on # of
receptors activated).

60
Q
Minimal adaptation 
and a nociceptors 
activity actually 
--- if the 
painful stimuli 
continues 
(hyperalgesia) due 
to nociceptor 
sensitization
A

INCREASES

61
Q

Allodyina

A

painful
sensation to a
innocuous stimulus

can occur too

62
Q
“Stimulation of nociceptors also 
leads to antidromal (reverse) 
activation of nociceptive nerve 
terminals and release of 
(2). Release 
of these peptides causes (5)
A

substance P and calcitonin gene related peptide

mast 
cell degranulation, vasodilation 
and edema, and further 
sensitization and activation of 
nociceptors (neurogenic 
inflammation).”
63
Q

Triple Response (3)

A
1. Red flush around site of 
injury (flare)
2. Local tissue edema
3. Sensitization to noxious 
stimuli
64
Q

Tissue injury leads to local release of — that excite or sensitize nociceptors causing —

A

endogenous inflammatory mediators (ex.
Histamine, Prostaglandins, Bradykinin, etc.)

Hyperalgesia

65
Q

Aδ Fibers:

A

Small, Myelinated, 12-30 m/sec (fast)
– Neurotransmitter includes Glutamate
– Sharp, localized pain (FAST PAIN)
– Thermal and Mechanical Stimuli

66
Q

C Fibers:

A
Unmyelinated, 0.5-2 m/sec (slow)
– Neurotransmitter includes Substance P
– Dull, diffuse pain (SLOW PAIN)
– Thermal, Mechanical and Chemical 
Stimuli
67
Q

The second order neuron crosses
over in the — — to
the opposite side of the spinal cord
to ascend contralaterally.

A

anterior commissure

68
Q

divisions of the Spinothalamic Tract (2)

A

Neospinothalmic

Paleospinothalamic

69
Q

Neospinothalmic:

A

Mostly A delta fibers. Provides location, intensity, & duration information.

70
Q

Paleospinothalamic:

A

Mostly C fibers. Some of these fibers synapse with brainstem structures (Reticular Formation, Periaqueductal Gray Region, Limbic System, Hypothalamus) and also with diffuse areas of the cortex for poorly localized sense of pain.

71
Q

There are multiple alternate pathways: (3)

i. Spinoreticular pathway. Mediates
ii. Spinomesencephalic pathway. Activates
iii. Spinohypothalamic pathway. Activates

A

arousal & autonomic responses
anti-nociceptive, descending pathways
the hypothalamus

72
Q

The Spinothalamic Pathway includes the

A

Neospinothalamic and Paleospinothalamic

Tracts

73
Q

Spinothalamic Pathway

First Order Neuron:

A

cell body in dorsal root
ganglion (or somatic afferent ganglion of cranial
nerves).

74
Q

Spinothalamic Pathway

Second Order Neuron:

A

cell body is in dorsal
nuclei & axons decussate via the anterior
commissure and terminate in thalamus. Can be
solely nociceptive OR Wide-Dynamic Range
(WDR) neurons.

75
Q

Spinothalamic Pathway

Third Order Neuron:

A

cell body in thalamus,
axons project to the sensory cortex. Sensory
Homunculus

76
Q

First- and Second-Order Neurons

Synapse in the

A

Dorsal Horn of the Spinal

Cord

77
Q

Spinal cord gray matter was divided
by Bror Rexed in the 1950s into ten
—. I-VI are in the dorsal horn.

A

laminae

78
Q

Second-order neurons in the

dorsal horn are either:

A
  1. Nociceptive-specific
    Neurons
  2. Wide Dynamic Range (WDR)
    Neurons
79
Q

Nociceptive-specific neurons

receive

A

only noxious stimuli

80
Q

WDR neurons also receive

A

non-
noxious afferent input from Aβ, Aδ,
and C fibers

81
Q
--- neurons are the 
most prevalent cell 
type in the dorsal horn 
(most abundant in 
Lamina V).
A

WDR

82
Q

Wide Dynamic Range Neuron

A
During repeated stimulation, 
WDR neurons characteristically 
increase their firing rate 
exponentially (wind-up), even 
with the same stimulus 
intensity. They have larger 
receptive fields than 
nociceptive-specific neurons.
83
Q

Nociceptive Specific Neuron

A
Found in lamina I and have 
discrete, somatic receptive 
fields; they are normally silent 
and respond only to high-
threshold noxious stimulation, 
poorly encoding stimulus 
intensity.
84
Q

Mechanisms for CENTRAL Modulation of Pain (3)

A

Facilitation of Pain
1. Wide-Dynamic Range (WDR) Neurons found in the dorsal horn
of the spinal cord. They respond to all somatosensory
modalities. Normally only sensitive to non-noxious stimuli
UNLESS the stimulus is highly noxious.
Allodynia = Perception of non-noxious stimuli as pain
2. Receptor Field Expansion of dorsal horn neurons so adjacent
neurons become responsive to stimuli (whether noxious or not)
3. Some second order neurons increase their frequency of
activation following prolonged discharge—”wind-up.” May
continue, even after the nociceptive stimulus is removed.

85
Q

Mechanisms for CENTRAL Modulation of Pain

Inhibition of Pain (2)

A

gate control theory of pain

pain inhibits pain

86
Q

Gate Control Theory of Pain:

A

Activation of Ab fibers from the same
region inhibits the Spinothalamic pathway
and reduces pain perception

The A-β fibers activate an inhibitory
interneuron that causes post-synaptic
inhibition of the Second-order neuron for
the Pain Pathway. This inhibition leads to
a weaker pain signal being sent to the
thalamus and somatosensory cortex.

This is the basis for how massage therapy
and TENS units work as a treatment for
chronic pain conditions and is why rubbing
a painful region makes it feel better.

87
Q

Pain Inhibits Pain

A
Stimulate pain in other regions of 
the body to inhibit pain (via 
GABA) at second order, WDR, 
neurons in spinal cord (Diffuse 
Noxious Inhibitory Control 
(DNIC) or Conditioned Pain 
Modulation (CPM))
88
Q

Conditioned Pain Modulation

CPM

A

a second noxious stimulus leads to the activation of PAG, NRM and RVM in the brainstem, which results in diffuse analgesic effect over the rest of the body.
“Pain Inhibits Pain”

Interneurons in the dorsal horn of the spinal
cord are activated by 5-HT/NE and release
endogenous opiates (Enkephalin).
Enkephalin in the dorsal horn inhibits the
first-order and second-order neurons
(nociceptive specific and/or WDR neurons).

89
Q

In —, there is evidence of
low concentrations of serotonin and
NE in the CSF, which suggests this
pathway might have reduced activity.

A

Fibromyalgia

90
Q

Analgesia is the

A

selective suppression of pain without

effects on consciousness or other sensations.

91
Q

We use many mechanisms to achieve pain relief: (5)

A
  1. Pharmacological agents: COX Inhibitors (aspirin,
    ibuprofen), Opioids, Antidepressants (TCAs),
    Anticonvulsants (GABApentin), Topical Lidocaine
    & Capsaicin
  2. Massage (Gate Control Theory of Pain)
  3. Acupuncture (seems to be linked to activation of
    the endogenous opioid pathways)
  4. Transcutaneous Electrical Stimulation (TENS)
  5. Nerve Blocks
92
Q

Pain information from the orofacial region is

conveyed into the CNS via the (2)

A

Trigeminospinothalamic Tract and the

Trigeminoreticular Tract

93
Q

Pain can be referred to the orofacial region

particularly teeth) in response to: (5

A
  • Maxillary Sinusitis
  • Angina
  • Migraine
  • Nasal Mucosa
  • Ear Pain
94
Q

It is often difficult to – tooth pain.

A

localize

95
Q

Dentin and enamel has limited space to swell in the
— state, so results in

A

inflammatory

exaggerated pain even with mild inflammation

96
Q

Painfully noxious hot/cold stimuli do not cause pain in an
uninflamed healthy tooth due to thermal insulating of the
enamel. But, with missing enamel and exposed dentin, a
slight thermal stimuli will cause

A

sudden and stinging pain.
– It is difficult to distinguish between between noxious hot
or cold stimuli.

97
Q

Weak air puffs to exposed dentin result in

A

intense pain

while in skin this would result in the sensation of light touch.

98
Q

Stimulation of tooth pulp by any kind of stimulus results in a

A

painful sensation

99
Q

While afferent fibers innervating teeth comprise only 0.1% of
trigeminal neurons, each of these fibers has extensive branching,
such that each afferent nerve innervates

A

multiple teeth.

100
Q

Large receptive fields =

A

Poor Localization

101
Q

The pulp is highly innervated with sensory afferents, mostly for pain, but the dentin has limited innervation but is sensitive due to

A

dentinal tubules.

Nerve fibers penetrate the dentinal tubules, but only for a short distance into the inner dentin.

102
Q

Odontoblasts have long processes that are located in the — — and their cell body is on the surface of the — —

A

dentinal tubule

dental pulp

103
Q
Studies have shown 
that sensitive teeth 
have many more (8X) 
and wider (2X) 
--- ---
compared to non-
sensitive teeth. --- ---
 thought to be 
more important than 
number since flow is 
proportional to the 
fourth power of the 
radius.
A

dentinal tubules
Tubule
radius

104
Q

Tissue is highly vascular, contains many neurons, but is a

— tissue because it is surrounded by

A

low-compliance

hard tissue

105
Q

Any change in volume within the tooth pulp translates to large
changes in pressure (3)

A

a. Inflammation due to mechanical or bacterial trauma
b. Increases in pulpal temperature secondary to laser radiation
c. Can lead to hypoxia and eventually tissue necrosis

106
Q

Dentin is a mineralized, avascular tissue (3)

A

a. Suprasensitive to extreme temperatures, particularly at the neck
of the tooth (gingival recession, wear of cementum and enamel)
b. Sensitive to hyperosmotic solutions
c. NOT sensitive to KCl, bradykinin, and histamine

107
Q

Dentinal tubules contain odontoblasts and perhaps they also

contain

A

nerve terminals

108
Q

The mechanism of — — in dentin is not currently

understood.

A

pain transduction

109
Q
Dentinal and pulp nociceptor 
information travels via Aδ 
and C fibers along with Aβ.   
The nerve fibers in tooth pulp 
are ~90%
A

C-fibers

110
Q

Dentinal Pain:

A

sharp pain

111
Q

Pulp Pain:

A

dull pain

112
Q

Dentin and Pulp are separated

by

A

tight junctions between
epithelial cells—selectively
permeable barrier

113
Q

Neural Theory

A
Free nerve 
endings in 
dentinal 
tubules are 
activated
114
Q

Hydrodynamic Theory

A
Stimulus displaces 
fluid in dentinal 
tubules which 
activates 
mechanoreceptors in 
nerve endings of 
dentin or pulp.
115
Q

Odontoblast

Transducer Theory

A
Odontoblasts 
are excited 
and transduce 
the signal to 
nearby nerve 
cells
116
Q

TRPV1

A
Polymodal receptor activated by 
painful chemicals (Capsaicin) and 
noxious temperatures (above 42°C)
117
Q

TRPM8

A

Low Temperature (threshold 25°C)

118
Q

TRPA1

A
Low Temperature (threshold 17°C)
Mechanosensation?
119
Q

The periodontal ligament has (2)

A
nociceptors AND 
Ruffini Endings (a mechanoreceptor/proprioceptor).
120
Q

Periodontal nociceptive information from free

nerve endings travels via

A

Aδ/C fibers

121
Q
The --- --- regulate the forces 
applied by the teeth in occlusion, 
mastication and biting. These receptors 
are slowly adapting, show directional 
sensitivity and their response varies 
with the force applied to the tooth.
A
periodontal mechanoreceptors 
(Ruffini endings)
122
Q

Subjects with dentures (who lack corresponding
PDL receptors), show impaired – —-
perception in tasks as biting force discrimination

A

intraoral sensory

123
Q

the apical portion of the
periodontal ligament is the
most heavily —

A

innervated