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DPT 520 > Exam 1 > Flashcards

Exam 1 Flashcards

Quiz 1 and this content

1
Q

where is a medial medullary lesion?

A

in the rostral medulla

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2
Q

what is the pattern of sensory loss with a medial medullary lesion?

A

contralateral loss of discriminative touch and proprioception in the body

no loss of somatosensation in the face

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3
Q

why is there no loss of somatosensation in the face with a medial medullary lesion?

A

bc the trigeminal light touch pathways decussate at the pons above the medulla and goes back up

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4
Q

what is the pattern of somatosensory loss in bilateral polyneuropathy?

A

“glove and stocking” loss of all modalities following the order of sensory loss bilaterally

starts peripherally and doesn’t affect proximal structures

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5
Q

what is the order of sensory loss?

A

proprioception, light touch, cold, fast pain, heat, slow pain

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6
Q

what is the pattern of somatosensory loss with a peripheral nerve lesion?

A

sensory loss in specific areas that follows the peripheral nerve distribution

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7
Q

what are some examples of peripheral nerve lesions?

A

carpal tunnel syndrome

sciatica

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8
Q

what is the difference b/w a nerve root lesion and a peripheral nerve lesion?

A

a nerve root lesion will follow the dermatomal pattern of loss and covers a larger area

a peripheral nerve lesion follows the peripheral nerve distribution which tends to be a smaller area

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9
Q

what is the pathophysiology of shingles?

A

retraction of the herpes zoster virus (chickenpox) in the DRG or sensory ganglia of the CN causes inflammation of the affected nerves

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10
Q

what is the pattern of somatosensory loss in shingles?

A

dermatomal bc it affects the nerve root

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11
Q

shingles usually affects the ______ dermatome

A

thoracic

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12
Q

does shingles causes sensory or motor loss or both?

A

always sensory loss bc the lesion is in the DRG or trigeminal nucleus

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13
Q

what are the s/s of shingles?

A

eruption of vesicles/clusters of blisters

itching and/or tingling (usually the first sign)

severe burning pain (can last up to 4 wks)

post herpetic neuralgia

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14
Q

what is usually the first s/s of shingles?

A

itching/tingling

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15
Q

t/f: shingles is usually limited to one or two dermatomes

A

true

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16
Q

is shingles unilateral or bilateral?

A

unilateral

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17
Q

what can shingles s/s develop into?

A

post herpetic neuralgia

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18
Q

what is post herpetic neuralgia?

A

sharp, electric-shock like pain following the path of the nerve root that can last after the initial s/s are gone

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19
Q

what is the PT’s role in management of shingles?

A

TENS over nerve root and/or one above or below it to treat the lasting nerve pain

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20
Q

what is pain?

A

unpleasant physical and emotional experience which signifies tissue damage or the potential for such damage

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21
Q

pain is a ____ and the emotional response to the _____

A

perception, perception

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22
Q

t/f: pain can result from structural changes in the NS

A

true

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23
Q

what causes nociceptive pain?

A

stimulation of free nerve endings

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24
Q

t/f: stimulation of free nerve endings always reaches the brain

A

false

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25
Q

perception of pain is always in the ____, not in the _____

A

brain, periphery

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26
Q

t/f: pain is just a physical experience

A

false

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27
Q

t/f: pain alters physical and psychological processes

A

true

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28
Q

nociceptors are activated by ______ stimulus and activation of the _____ _____ _____ _____

A

mechanical, 1st order nociceptive neuron

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29
Q

what are the ascending pathways of pain?

A

spinothalamic tract

divergent pathways (spinomesencephalic, reticulospinal, spinolimbic)

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30
Q

what are the divergent pathways?

A

spinomesencephalic, reticulospinal, and spinolimbic

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31
Q

what ascending pathway is well localized fast, discriminitive pain?

A

spinothalamic

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32
Q

what ascending pathway is slow aching, interpretive pain?

A

the divergent pathways

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33
Q

what is the pain matrix?

A

areas of the brain and NS activated when there’s a pain response

network of brain areas that process and regulate pain info

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34
Q

what is the pain response?

A

something that triggers descending pathways activation

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35
Q

t/f: the pain matrix can create pain perception w/o nociception

A

true

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36
Q

how does the pain matrix create pain w/o nociception?

A

activation of an area creates pain w/o peripheral input

maladaptive rewiring of the brain areas involved

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37
Q

what tract is the lateral system of the pain matrix?

A

the spinothalamic tract

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38
Q

what tract is the medial system of the pain matrix?

A

the divergent pathways

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39
Q

where in the cortex is the lateral system of the pain matrix?

A

primary sensory cortex

insula

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40
Q

where in the cortex is the medial system of the pain matrix?

A

insula or insular lobe

anterior cingulate cortex (ACC)

pre-frontal cortex

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41
Q

what are the subcortical structures of the medial system of the pain matrix?

A

amygdala

hypothalamus

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42
Q

where in the thalamus is the lateral system of the pain matrix?

A

VPL/VPM

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43
Q

where in the thalamus is the medial system of the pain matrix?

A

midline

intralaminar nuclei

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44
Q

where in the brainstem is the medial system of the pain matrix?

A

periaqueductal gray

reticular formation

ventral medulla

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45
Q

what is the lateral system of the pain matrix?

A

discriminative info about location, timing, and intensity of pain/damage

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46
Q

what does the insula contribute to?

A

cognitive, evaluative interpretation of the pain; strong connection to the limbic system

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47
Q

what is the role of the medial system of the pain matrix?

A

to provide meaning to the pain; emotional interpretation

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48
Q

what is the role of the anterior cingulate cortex (ACC)?

A

complex cognitive processing

impulse control

sympathy/empathy

decision making

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49
Q

what is the role of the pre-frontal cortex?

A

decision making

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50
Q

which system of the pain matrix has more connections in the brain?

A

the medial system

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51
Q

what is the role of the amygdala?

A

to ascribe meaning to the pain

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52
Q

what is the role of the reticular formation?

A

to direct attention to the pain

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53
Q

what is the role of the PAG?

A

release of endogenous opioids that have an important role in modulating pain (suppression of pain)

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54
Q

what are the 3 pain responses?

A

reflex movements

autonomic responses

muscles guarding

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55
Q

what are reflex movements?

A

removing the limb from the painful stimuli

w/drawal reflex

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56
Q

what are the autonomic responses?

A

increased internal temperature

increased BP

increased HR

increased RR

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57
Q

what is muscle guarding?

A

reflex to protect the area

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58
Q

the pain matrix generates a ____ ____ response to regulate/modulate pain signals

A

top down

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59
Q

what is antinociception?

A

transmission of nociceptive info that can be suppressed at several locations in the NS

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60
Q

what are the 5 levels of antinociception from most peripheral to most cortical?

A
  1. periphery
  2. dorsal horn
  3. neuronal descending system
  4. hormonal system
  5. amygdala and cortical level
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61
Q

how does antinociception work in the periphery?

A

decreased activation of nociceptors and 1st order nociceptor fibers

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62
Q

what are examples of peripheral antinociception?

A

anti-inflammatory drugs

topical menthol rubs and capsaicin

local anesthetics

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63
Q

how do anti-inflammatory drugs work?

A

they decrease the synthesis of prostaglandins that are created from arachidonic acid in the inflammatory response

pain is decreased bc the 1st order neuron isn’t activated as much

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64
Q

how do topical menthol rubs and capsaicin work?

A

they desensitize nociceptive fibers

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65
Q

how do local anesthetics decrease pain?

A

they block Na+ channels in neurons to prevent APs (opening of Na+ channels is what initiates APs)

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66
Q

how does antinociception work in the dorsal horn?

A

decreased relay of nociceptive info to 2nd order neurons

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67
Q

what are examples of antinociception in the dorsal horn?

A

gate-theory/counterirritant theory

high frequency, low intensity TENS

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68
Q

what is gate theory/counterirritant theory?

A

in modulated pain, A beta fibers (DCML) synapses on and excites the inhibitory interneuron on the C fibers for pain

mechanical info that isn’t pain activates the inhibitory interneuron to lessen pain

the use of an inhibitory interneurons as a gate

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69
Q

what is high-frequency, low intensity TENS?

A

treatment of non-chronic LBP

fast frequency competes with the pain signal to lessen it’s effects

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70
Q

how does antinociception work in the fast-acting neuronal descending system?

A

the PAG activates the ventromedial medulla which activates the raphespinal tract to release serotonin to block pain transmission and lessen pain

the locus coerulus releases NE to inhibit spinothalamic activity and suppress the release of nociceptive transmitters

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71
Q

what structures are involved in the fast acting neuronal descending system?

A

PAG

rostral ventromedial medulla

raphespinal tract

locus coerulus in the pons

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72
Q

how does the ceruleospinal tract inhibit spinothalamic activity?

A

binds to afferent nociceptive neurons to suppress APs

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73
Q

how does antinociception work with hormonal control?

A

endogenous analgesic hormones (endogenous opioids) are released by the periventricular zone (PVZ), pituitary gland, and adrenal medulla

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74
Q

where are the receptors for endogenous opioids?

A

PAG

rostral ventromedial medulla

dorsal horn

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75
Q

what are the endogenous opioids?

A

endorphin, enkephalin, and dynorphin

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76
Q

how do we activate the hormonal controls?

A

with pain

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77
Q

what are ways the hormonal controls are used?

A

low-frequency, high-intensity TENS

runner’s high

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78
Q

how does low-frequency, high-intensity TENS work?

A

it activates mechanoreceptors and nociceptive fibers

controlled discomfort to treat chronic pain

endogenous opioids system kicks in with nociceptive stimulation

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79
Q

why is low-frequency, high-intensity TENS used to treat chronic pain?

A

bc you can’t just stimulate mechanoreceptors to relive their pain as the pain isn’t nociceptive, it has to be higher up

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80
Q

how does runner’s high work in the hormonal control system?

A

the endogenous analgesic hormones system is activated and released opioids to suppress pain

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81
Q

what is stress induced antinociception?

A

stress suppressing nociceptive pain with the activation of the sympathetic NS in response to pain

activation of the raphespinal tract and PVZ w/ the release of endogenous alalgestics that bind to opioid receptors in the pain matrix and SC

82
Q

how does antinociception in the amygdala and cortex work?

A

it is responsible for the emotional aspects of pain

83
Q

what happens at the amygdala level of antinociception?

A

emotional aspects of pain where upsetting experiences outside of pain makes pain worse

84
Q

what happens at the cortical level of antinociception?

A

expectations, distraction, and placebo can suppress pain

85
Q

what is pronociception?

A

increased pain intensity

86
Q

what are the 3 levels of pronociception?

A
  1. periphery
  2. psychiatric influence
  3. pain matrix
87
Q

what is peripheral pronociception?

A

edema and endogenous chemicals sensitize free nerve endings

88
Q

increased edema=____ pain

A

increased

89
Q

what is the psychiatric influence of pronociception?

A

stress, anxiety, and depression intensify pain

90
Q

how does the pain matrix contribute to pronociception?

A

it can produce pain in the absence of nociceptive input

91
Q

what is normal sensory processing in the dorsal horn?

A

perceiving nociceptive info as nociceptive

92
Q

what is suppressed sensory processing in the dorsal horn?

A

gate control theory

use of high-frequency, low-intensity TENS

93
Q

what is sensitized (acute) sensory processing in the dorsal horn?

A

pain w/o nociceptive input

increased NT=increased receptor binding

94
Q

what is reorganized (persistant) sensory processing in the dorsal horn?

A

long term potentiation

structural changes resulting in persistant increase in sensitivity

allodynia vs hyperalgesia

95
Q

what is acute pain?

A

nociceptive pain from a nociceptive stimulus leading to a potential/actual tissue damage

96
Q

what is chronic pain?

A

pain most/every day for the past 3 months

can be nociceptive or non-nociceptive

97
Q

can the pain in nociceptive chronic pain be eliminated when the trigger is eliminated?

A

yes!

98
Q

what are types of non-nociceptive chronic pain?

A

neuropathic pain

central sensitivity syndromes

pain syndromes

99
Q

t/f: there is no active tissue injury in non-nociceptive chronic pain

A

true

100
Q

what is somatic pain?

A

localized pinprick, stabbing, or sharp pain from a delta fiber activity in the periphery

101
Q

what is visceral pain?

A

generalized aching, pressure, or sharp pain from c fiber activity and involved deeper innervation

102
Q

what is neuropathic pain?

A

radiating or specific pain described as burning, prickling, tingling, electric shock-like, or lancinating pain from dermatomal or non-dermatomal mechanisms

103
Q

what is central pain?

A

thalamic pain

104
Q

what kind of pain is associated with MS, GBS, and carpal tunnel syndrome?

A

neuropathic pain

105
Q

what are some causes of nociceptive pain?

A

burns

mechanical LBP

cancer

arthritis

trauma

metabolic disease

infection

soft tissue injuries

106
Q

what is referred pain?

A

pain at another location from the actual site of origin

inflammation of the viscera and the brain’s misinterpretation of the nociceptive signal

107
Q

what pain requires a referral somewhere else when presented in PT?

A

referred pain

108
Q

what are the symptoms of neuropathic pain?

A

paresthesia

dysesthesia

allodynia

hyperalgesia

109
Q

what is paresthesia?

A

numbness

110
Q

what is dysesthesia?

A

abnormal sensation

111
Q

what is allodynia?

A

pain w/non-nociceptive signals

112
Q

what is hyperalgesia?

A

excessive pain response to nociceptive signals

113
Q

what are the 4 mechanisms that produce neuropathic pain?

A

ectopic foci

ephaptic transmission

allodynia

hyperalgesia

114
Q

what is ectopic foci?

A

demyelinated axon creates AP itself

very sensitive channels that fire APs w/o stimulation from the soma

115
Q

what is ephaptic transmission?

A

abnormal signaling b/w adjacent demyelinated axons w/o synapses

cross-talk

116
Q

what cellular changes are associated with central sensitization?

A

increased spontaneous activity with no stimulus

increased responsiveness to afferent inputs due to a lowered activation threshold

prolonged after-discharge in response to repeated stimuli

expansion of receptive fields to a greater area around the injury

117
Q

what sites generate neuropathic pain?

A

periphery

dorsal horn

CNS

118
Q

what damages to neurons can cause neuropathic pain?

A

stroke

diabetes

MS

viral infection (GBS)

119
Q

what are the peripheral generations of neuropathic pain?

A

complete or partial damage to a nerve

120
Q

what does complete nerve severance cause?

A

lack sensation from the nerve’s receptive field

sometimes paresthesia and pain

121
Q

what does partial damage to a nerve cause?

A

allodynia

electric shock-like sensations

122
Q

what causes peripheral neuropathic pain?

A

ectopic foci and ephaptic transmission

123
Q

what is tinel’s sign?

A

tapping an injured nerve can elicit pain/tingling

mechanical stimulus elicits pain

124
Q

what is deafferentation?

A

disruption in afferent fibers and signals

125
Q

when peripheral sensory information is completely absent, neurons in the CNS that formerly received information from the body part may become _____ ______

A

abnormally active

126
Q

what are the central responses to deafferentation?

A

phantom pain

central pain

small fiber neuropathy

127
Q

what is phantom pain/sensation?

A

pain coming from a limb that is no longer there due to structural reorganization that occurs

128
Q

what allows a cut axon to still send potentials?

A

ectopic foci and ephaptic transmission

129
Q

what is a common treatment of phantom sensation?

A

mirror therapy

130
Q

what is central pain caused by?

A

CNS lesion

131
Q

what is central pain?

A

an area of the body deafferentated by a lesion causing burning, shooting, aching, freezing, tingling pain

similar to phantom sensation

132
Q

what are causes of central pain?

A

SCI

stroke

MS

133
Q

how does a SCI lead to central pain?

A

spontaneous activity of the VPL thalamic nucleus (spinothalamic and DCML)

134
Q

when does a stroke lead to central pain?

A

following a lateral medullary lesion or ventroposterior thalamic lesion

135
Q

what is small fiber neuropathy?

A

damage to C fibers and loss of nociceptors

partial deafferentation and central sensitization

136
Q

what are some examples of small fiber neuropathies?

A

polyneuropathies

post herpetic neuralgia

137
Q

what do central sensitivity syndromes do?

A

disrupt top-down regulation of pain

decreased antinociception

increased pronociception

138
Q

what set of symptoms occur in central sensitization syndromes?

A

hypersensitivity to lights, sounds, touch, and scents

139
Q

what are the 4 central sensitization syndromes?

A

fibromyalgia

episodic tension type headache

migraine

chronic whiplash associated disorder

140
Q

what is fibromyalgia?

A

increased glutamate in the SC leads to amplified neural responses

decreased pain inhibition

141
Q

what are the s/s of fibromyalgia?

A

widespread pain and stiffness

fatigue

impaired concentration and memory

impaired sleep

functional impairment

142
Q

what is an episodic tension type headache?

A

bilateral supersensitivity of the nociceptive pathway to nitric oxide (vasodilation/constriction)

moderate

triggered by fumes, mold, light, or noise

no nausea or vomiting

143
Q

t/f: episodic tension type headaches often involved nausea and vomiting

A

false

144
Q

what are migraines?

A

unilateral hypersensitivity and amplification of nociceptive signals in the trigemino-thalamo-cortical pathway

severe pulsating

145
Q

what are the s/s of a migraine?

A

nausea, vomiting, photophobia (light sensitivity), and/or phonophobia (noise sensitivity)

146
Q

what is chronic whiplash associated disorder?

A

allodynia and hyperalgesia around the neck exacerbated by cervical movements

overstretch of nerves/shear force to nerves combined with tissue vulnerability

147
Q

t/f: chronic whiplash associated disorder can be worsened by stress

A

true

148
Q

what are red flags with headaches?

A

onset of paralysis/reduced level of consciousness

149
Q

what are the signs that a headache may be caused by excessive intracranial pressure?

A

headache present at waking

pain triggered by coughing, sneezing, or straining

vomiting

worse when lying down

150
Q

what are signs that a headache may be caused by serious intracranial disease (encephalitis, meningitis)

A

progressive worsening over days or weeks

necks stiffness and vomiting

rash and fever

history of cancer or HIV infection

151
Q

what are signs that a headache may be caused by hemorrhage?

A

headache following head injury

abrupt onset

history of HTN and hyperglycemia

152
Q

what are pain syndromes?

A

involve other body systems in addition to the pain system

disorder/dysfunction of anti/pronociception

153
Q

what are 2 examples of pain syndromes?

A

CRPS

chronic LBP syndrome

154
Q

what is CRPS?

A

progressive regional pain syndrome affecting somatosensory, autonomic, and motor systems following trauma

155
Q

what are the s/s of CRPS?

A

vascular and trophic changes

muscle atrophy

edema

156
Q

what is the primary precipitating factor for CRPS?

A

disuse of limbs

157
Q

what is stage 1 CRPS?

A

severe burning/aching pain that increases w/ slight touch/breeze

fluctuation in skin temp

rapid growth of hair and nails

changes in skin color, appearance, and texture (pale, red, blotchy, thin, and dry)

hyperhydrosis (excessive sweating)

158
Q

what is stage 2 CRPS?

A

increased level of pain

continued skin changes (blue, cold, shiny, dry, and flaky)

brittle and cracked nails

hair growth slows down

stiff joints

muscle weakness

lasts 3-6 months

159
Q

what is stage 3 CRPS?

A

too painful to move affected limb

muscle atrophy of affected limb

arthritic changes

very blue, thin, shiny skin

involvement spreads through entire limb

osteoporosis

160
Q

what are aggregating factors of CRPS?

A

psychologic and physiologic stimuli

161
Q

what is chronic LBP syndrome?

A

change in LBP etiology from tissue damage to central sensitization and deconditioning

162
Q

what are s/s of chronic LBP syndrome?

A

pain matrix dysfunction

muscle guarding

abnormal movement

disuse atrophy

decreased pain threshold

163
Q

what can be done at the cortical level to manage chronic LBP syndrome?

A

placebo, distraction, positive outlook and expectations, and motivation

164
Q

what can be done at the hormonal level to manage chronic LBP syndrome?

A

endogenous opioid release with exercise

165
Q

what are the sex differences in pain perception?

A

women are more sensitive to pain than men

women are at a greater risk for developing chronic pain

166
Q

what may account for the differences in pain perception b/w the sexes?

A

hormones-testosterone is associated with opiate-mediated pain relief

167
Q

_____ lean mass may alleviate pain by _____ ascending nociceptive signals

A

increased, decreasing

168
Q

where are the cell bodies of LMNs located?

A

in the ventral horn of the SC

169
Q

a lesion inside the foramen would lead to a _____ pattern of loss

A

dermatomal/myotomal

170
Q

a lesion outside the foramen would lead to a _____ pattern of loss

A

peripheral

171
Q

what are the signs of a LMN lesion?

A

hypotonicity

decreased/loss of reflexes (hyporeflexia)

neurogenic atrophy

fasciculation/fibrillation

paralysis and paresis

172
Q

what is muscle tone?

A

resistance to muscle stretch in resting muscle

173
Q

what factors contribute to muscle tone?

A

descending motor commands

proprioceptive info

weak cross bridge binding

titan

174
Q

what is hypotonia?

A

low muscle tone

abnormally low resistance to passive motio

resting tension is close to none

175
Q

what is flaccidity?

A

more severe absence of resistance to passive movement

176
Q

why can hypotonicity lead to injury?

A

ligament laxity and hypermobility puts the joints at risk for injury

lack of voluntary motor control

177
Q

what 2 things can phasic stretch reflex/DTR determine?

A
  1. determine integrity of monosynaptic reflex and SC at dif segmental levels
  2. determine excitability of the alpha motor pool
178
Q

diminished input from motor neurons to skeletal muscles leads to what?

A

hyporeflexia

179
Q

what is neurogenic muscle atrophy?

A

loss of muscles bulk due to motor neuron axons dying so that there is no nerve stimulus to muscles

denervation of skeletal muscles

180
Q

what is neurogenic muscle atrophy associated with?

A

LMNs

181
Q

is neurogenic muscle atrophy rapid or slow?

A

rapid

182
Q

why does denervation occur in neurogenic muscle atrophy?

A

bc the ground motor neuron is trying to innervate a lot more fibers and it can’t support them so they die leaving only one type of fibers

183
Q

what is the series of events in neurogenic muscle atrophy?

A

lack of neural stimulation and contraction–>lack of gene expression–>changed protein production–>rapid atrophy

184
Q

what will a muscle biopsy show in LMN lesion?

A

change in protein production in the muscle

185
Q

what is fasciculation?

A

spontaneous quick twitch of single motor unit (one motor neuron and all fibers it innervates) that can be seen

186
Q

t/f fasciculation is always pathologic

A

false, it is only pathologic when there is atrophy

187
Q

what may cause fasciculation?

A

too much caffeine

fatigue

188
Q

what is fibrillation?

A

spontaneous contraction of muscles fibers that can’t be observed with the eyes

dispersed ACh receptors (bc of muscles not getting enough ACh) become hypersensitive to any ACh

189
Q

t/f: fibrillation is always pathologic

A

true

190
Q

what is fibrillation a sign of?

A

denervation/electrolyte imbalance

191
Q

what is the difference b/w paralysis and paresis?

A

paralysis: completely severed nerve with no way of signals to get to muscles

paresis: cut a few fibers weakening muscles

192
Q

how do we measure muscle strength?

A

MMT and dynamometer

193
Q

what movement is produced by the C5 myotome?

A

elbow flexion

194
Q

what movement is produced by the C6 myotome?

A

wrist extension

195
Q

what movement is produced by the C7 myotome?

A

elbow extension

196
Q

what movement is produced by the C8 myotome?

A

flexion of the tip of the middle finger

197
Q

what movement is produced by the T1 myotome?

A

finger abduction

198
Q

what movement is produced by the L2 myotome?

A

hip flexion

199
Q

what movement is produced by the L3 myotome?

A

knee extension

200
Q

what movement is produced by the L4 myotome?

A

ankle dorsiflexion

201
Q

what movement is produced by the L5 myotome?

A

great toe extension

202
Q

what movement is produced by the S1 myotome?

A

ankle plantarflexion

DPT 520 (13 decks)

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