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PTRS 852 - Neuro PT I Midterm > Pain > Flashcards

Pain Flashcards

1
Q

Describe the PT’s goal for pain

A

Change the pt. perception of pain and restore function

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2
Q

3 Dimensions of Pain

A
  1. Sensory-discrimination (SENSORY)
  2. Motivational-affective (EMOTIONAL)
  3. Cognitive-evaluative (COGNITIVE)
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3
Q

Dimension of Pain: Location, magnitude, duration, quality

A

Sensory-discrimination

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4
Q

Dimension of Pain: Emotions, anxiety, depression

A

Motivational-affective

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5
Q

Dimension of Pain: post experience, possibility of outcomes, influenced by one’s culture and beliefs

A

Congitive-evaluative

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6
Q

Term: Increased sensitivity to noxious stimulus

A

Hyperalgesia

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7
Q

Term: Feeling of pain from a non-noxious stimulus

A

Allodynia

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8
Q

Describe the difference between primary and secondary pain

A

Primary - pain at the site of injury

Secondary - pain away from the site of injury, same as referred pain

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9
Q

Term: Increased responsiveness or decreased threshold of neurons

A

Sensitization

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10
Q

Describe the difference between peripheral and central sensitization

A

Peripheral = dysfunction in PNS, PRIMARY hyperalgesia/allodynia

Central = dysfunction in CNS, SECONDARY hyperalgesia/allodynia

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11
Q

Describe the basic concept of the Ascending Pain Pathways

A

3 order neuron system

1st order = primary afferent fibers (have two axons)

2nd order = spinothalamic tract

3rd order = thalamocortical neurons

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12
Q

Describe the difference between Alpha Delta/C fibers and Group 3/4 fibers

A

Alpha Delta and C fibers innverate the skin while Group 3/4 fibers innervate deep tissues (mm, joint, synovium, ligament, etc.)

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13
Q

Describe the difference between Alpha delta/G 3 pain and C/G 4 pain

A

Alpha beta/G 3 = fast, sharp pain from thermal or mechanical noxious stimulus; low-threshold

C/G 4 = slow, dull pain from thermal, mechanical or chemical noxious stimulus; high-threshold

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14
Q

Describe the difference between slow and fast pain

A

Fast: immediate sharp sensation and id of location; processed by lateral pain system (spinothalamic)

Slow: dull/burning/throbbing followed by sharp pain that is not easily localized; processed by medial pain system

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15
Q

Term: Sensory receptor that can transduce pain stimulus

A

Nociceptor

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16
Q

3 Types of pain processed by the PNS

A

Chemical, thermal, mechanical

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17
Q

Describe the noxious mechanical stimulus in the following tissue types

  1. Skin
  2. Visceral
  3. Joint
  4. Muscle
A
  1. cut, burn, stretch, pressure
  2. distension
  3. friction, pressure/compression, tension
  4. tear, stretch, ischemia
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18
Q

3 Peripheral Pain Mechanisms

A
  1. Uni/Polymodal neurons (indicates types of stimulus responded to)
  2. Receptors (ion channels and receptors)
  3. Chemical
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19
Q

2 Main functions of the Primary Afferent Neuron

A
  1. Transduction
  2. Transmission
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20
Q

Term: Detection of noxious or damaging stimuli

A

Transduction

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21
Q

Term: Passage of the resulting sensory input from peripheral terminals to spinal cord

A

Transmission

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22
Q

Describe why we can only have primary hyperalgesia/allodynia in the PNS

A

Because of the two main functions of the primary afferent

Can pain at location due to transduction but won’t transmit information to CNS due to damage

23
Q

Term: Tissue damage resulting in release of chemicals

A

Inflammation

24
Q

3 Sx of Inflammation

A
  1. Constant pain from normal stimuli
  2. Heat
  3. Edema
25
Describe the process that results in peripheral sensitization
After persistent inflammation there is up-regulation of ion and glutamate receptors The threshold for pain is lowered and there is increased synaptic activity Leading to increased responsiveness of peripheral nociceptors Finally phenotypic plasticity of nociceptors can occur (meaning nerves not meant to respond to pain begin to)
26
Describe neurogenic inflammation and its cause
Neurogenic inflammation occurs as a result of persistent inflammation. In this condition the neurons themselves are adding to the inflammation process by releasing glutamate
27
Describe the subjective and objective clinical findings for peripheral pain
SE: sx in nerve distribution, along n. trunk, hot spots along nerve, burning, sharp, night pain OE: neurodynamic testing, skin/temp changes
28
Describe the treatment for chemical and mechanical peripheral neurogenic pain
chemical: use of appropriate modalities, neurodynamic sliders, meds - NSAIDs mechanical: unload joint, change posture, look at ergonomics
29
3 Central pain mechanisms
1. Spinal mechanisms 2. Midbrain mechanisms (descending pathways) 3. Corticla mechanisms
30
Spinal pain mechanisms 1. Location 2. NT 3. Receptors
1. Dorsal Horn 2. Glutamate and Substance P (both excitatory) 3. NMDA receptors, NK receptors, Ca ion channels
31
3 Classifications of DH neurons and their location and effect
1. Projection n. -- part of spinothalamic tract in Rexed LI -- excitatory 2. Interneurons -- span Rexed LII-IV -- inbhititory 3. Wide dynamic range n. -- body in Rexed LV, span to Rexed LI -- excitatory or inhibitory
32
Describe the type of information sent to Rexed Lamina I-V
I, II, IV, V = pain information III, IV = tactile information
33
Describe what information type and to which Rexed Lamina the neurons send the informatin 1. Alpha Delta/G 3 2. C/G 4 3. Alpha Beta
1. Sharp pain with it's intensity and location to Rexed L I, IV, and V 2. Dull pain to Rexed L II 3. Pressure information to Rexed L III and IV
34
Describe the function and importance of Wide Dynamic Range Neurons
Function: Integrate painful/non-painful information received from both sides of the body and from multiple tissues/sites Importance: Are the reason for referred pain!! There is a convergence of input from various tissues and misinterpretation from the cortex resulting in referred pain
35
List the pathways of the lateral and medial pain system
Lateral = Lateral spinothalamic tract Medial = Anterior spinothalamic tract and spinolimbic tract
36
Main Descending Pain Pathway and its function
Periaqueductal gray-rostroventromedial medulla (PAG-RVM) of the midbrain Synapses directly and indirectly with the SC to modulate pain (typically inhibitory but can also be excitatory)
37
2 Locations Descending Pathways Modulate Pain
1. By blocking the signal at the central terminal of the 1st order neuron 2. By blocking the singal at the DH neurons (thus stopping the activation of the DH neurons)
38
5 Descending Pathway NT
1. Opiods (-) 2. Serotonin (-) 3. GABA (-) 4. NE (+/-) 5. Glutamate (+)
39
3 Inhibitory output and 2 excitatory output of the Descending PAthway
Inhibitory: electrical simulation, exercise, opioid meds Excitatory: increased glutmate release and tissue injury
40
Describe the Gate Control Theory
Describes the physiological mechanisms whil accounting for phsychological factors Overriding pain signals with non pain signals The balance between the periperhal nocicpetors and the other periperhal fibers stimulation as well as descending pain pathways leave the gate "open" or "closes" and modify your perception of pain
41
Describe the location of the gate and what opens and closes the gate
The "gate" is located in the DH Opened by: increased nociceptor activity, decreased activity of descending pathways - extent of injury, overstimulation to injured tissue, anxiety, depression, focusing on pain, linking to prior painful experience Closed by: increased activity of large afferents (i.e. Alpha Beta) and inhibitory descending pathways - medications, modalities conservative intervention, positive emotions, relaxation, meditation, distraction, involvement in other activities
42
Describe how DH neurons are sensitized (central sensitization)
The DH neurons up regulate and sprout axons/dendrites to Rexed L I, II, V Additonally there is production of genes, death of interneruons, and decreased descending pathway inhibition All of this leads to increased responsiveness of DH neurons to noxious and innocuous stimuli
43
Term: Brain regions that process and regulate pain information
Pain Matrix
44
Cortical areas that correspond to the following dimensions of pain 1. Sensory-discrimative 2. Motivational-affective 3. Cognitive-evaluative (4. Descending Control)
1. Thalamus and S1/2 2. Cerebrum (insula, cingulate, prefrontal cortex), Amygdala, Hypothalamus, Thalamus (ILN) 3. Prefrontal cortex 4. Brainstem and midbrain
45
Describe the type of system the pain matrix uses
Top-down Responds to acending pain signals after integrating sensory and affective pain regions to determine whether the information is normal or needs suppressed/amplified/reorganized
46
Describe the effects of central sensitization in the brain
1. Changes in the somatotopic arrangement (increased proportion given to area of sensitization) 2. Decreased brian chemicals essential to brain health (more glutamate and sub P, less inhibitory) 3. Loss of gray matter volume
47
Describe how the ANS can complicate pain
Contributes to emergency analgesia and provides E However, also adds to inflammation, causes DH sprouting and trophic skin changes
48
Describe the physiology behind persistent pain
- Upregulation of specific ion channels - Phenotypic switching of large myelinated axons - Sprouting within DH - Loss of inhibitory neurons - Misinterpretation by the brain
49
Type of Pain: Superficial or Deep pain
Somatic
50
Type of Pain: Associated with high anxiety or depression
Psychological
51
Results from distrubances in neural and non-neural cells that leads to maladaptive changes in the neurons and sensory system
Neuropathic
52
Type of Pain: Spontaneous nerve pain that is sharp/shooting/tingling, increased heat/cold sensitivity, increased pain perception
Neuropathic
53
List 5 Objective Pain Measures
1. McGill sensory and affective pain 2. Beck depression 3 Tampa kinesiophobia 4. Fear Avoidance 5. Oswestry disability (functional)
54
Describe the importance of CV fitness for (chronic) pain
It helps to stimulate the opiod system to control pain - mod intensity, 10-20 minutes, walking etc.

PTRS 852 - Neuro PT I Midterm (15 decks)

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