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pain neurology Flashcards

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1
Q

What is a facilitate segment?

A
  1. adverse neurologic response where a segment in lesion channels normal neural activity through efferent motor and sympathetic pathways
  2. Likened to a glass of water that is overflowing with neural activity and spilling out as excessive facilitation or inhibition to the corresponding segment
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2
Q

Who is created to the initial research into the facilitated segment?

A

In the 40s Korr, Denslow, Krems found region EMG activity with pressure to the spinous process

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3
Q

How are the facilitated segment and central sensitization related?

A
  1. Both are adverse neurologic activity

2. The facilitated segment however is not central sensitization and is still a peripherally driven process

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4
Q

What is allodynia?

A

Change in the central nervous system resulting in a heightened state of the nervous system where normal levels of afferent stimulus such as brushing or stroking cause the perception of pain.

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5
Q

What is the neurogenic inflammatory response?

A
  1. mechanical inflammation leads to a neurologic inflammatory response?
  2. involves vasodilatation and activation of inflammatory cells
  3. reduction in type IV thresholds or peripheral sensitization
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6
Q

What is peripheral sensitization?

A
  1. Decrease in free nerve ending threshold resulting in afferent signally from lower levels of mechanical, chemical or thermal stimulus
  2. The chemical mediators of inflammation reduce the threshold
  3. you can also have direct injury to the nerve that reduces its threshold
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7
Q

How can a peripheral nerve injury create peripheral sensitization?

A
  1. abnormal DH activity- increase type IV afferent flow causes wide range DH interneurons to lower their threshold
  2. Lower thresholds for the newly sprouted nerve endings
  3. Loss of c-fibers from injury leaves interneuron opening for developing new connection which may be type IVs
  4. ischemic demyelination leading to ectopic depolarization of nerves
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8
Q

What are the different classes of DH interneurons?

A
  1. Class I-low threshold activated by mechanorecptors
  2. Class 2 or wide range dynamic- activated by mechanoreceptor and nocioceptors
  3. Class 3- activated by nocioceptors
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9
Q

What class of DH interneuron is most likely responsible for transmitting conscience levels of pain?

A

Class II or wide range dynamic

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10
Q

What are projection neurons?

A

1.neurons in the spinal cord responsible for relaying an inhibitory or facilitory signal from one region to another region in the central nervous system

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11
Q

What projection neurons play a role in pain?

A
  1. spinothalamic tract- takes the signal from the DH to the thalamus
  2. descending control system effects the sensitivity of the DH
  3. local interneurons effect responsiveness of the DH to peripheral afferents
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12
Q

What are some examples of nerves that synapse on the class II or wide range dynamic DH interneurons?

A
  1. cutaneous type IV
  2. cutaneous type I and IIs
  3. deep connective tissues afferents
  4. organ afferents
  5. muscle spindle afferents
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13
Q

What is convergence within the DH?

A

the wide range dynamic interneurons are activated by both nociceptive and non-nociceptive afferent

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14
Q

What are the roles of the DH horn in the pain response?

A
  1. nocioceptive afferents terminate in laminas I and II
  2. DH is responsible for relaying the nociceptive signal via projection interneurons
  3. convergence of painful and normal neural activity occurs at the class II or wide range dynamic interneurons of the DH
  4. DH horn can become sensitized by a decrease in activation thresholds
  5. DH windup
  6. DH field expansion
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15
Q

How does the DH become sensitized to painful stimulus?

A

There are two process once the type IV send the nociceptive signal to laminas I and II

  1. spinothalamic activation causes the thalamus send descend stimulus to lower DH threshold
  2. there is an increase in local interneuron activity at the DH creating a reduction in thresholds
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16
Q

Is central sensitization of the DH horn a dysfunctional process?

A
  1. it is a normal response to pain

2. it can dysfunction if it becomes centrally mediated from chronic peripheral stimulation

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17
Q

What effect does the neurotransmitter have on the post synaptic membrane?

A
  1. it binds to the membrane creating a voltage change in the membrane
  2. voltage change will open ion channels by releasing the Mg++ block
  3. charged ions are then able to freely flow back and forth to create an inhibitory or an excitatory response
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18
Q

What ions create postsynaptic inhibition and excitation?

A
  1. inhibition is Cl-

2. excite is Ca+ or Na+

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19
Q

What neurotransmitters create a postsynaptic inhibitory effect with pain?

A
  1. Gamma Aminobutric Acid (GABA)

2. Glycine

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20
Q

What neurotransmitters create a postsynaptic excitatory effect?

A
  1. glutamate

2. aspartate

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21
Q

What are the postsynaptic excitatory receptors?

A
  1. N-methyl-D-Aspartate (NMDA)
  2. Non-MNDA- Kainate and AMPA
  3. Neurokin second messenger
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22
Q

What role does the excitatory second messenger system play in pain modulation?

A

produces a longer lasting effect in neural activity and it primes the NMDA receptors so there threshold is decreased

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23
Q

What effect does substance P have on the pain receptors of the DH

A

activates neuron receptors

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24
Q

What is DH windup?

A

changes in NMDA behavior in the DH lowering activation threshold following repeated stimulus of C-fibers less than 3 seconds apart

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25
Q

What is DH field expansion?

A

Neurons within the DH can expand their receptive field to include synapses with pathologic neurons so that facilitation of that neuron will now cause a pathologic response

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26
Q

What is proto-oncogenes role in the nervous system?

A
  1. substance believed to influence the process for central neural plasticity in development of chronic pain
  2. pathway:noxious stimulus -> influx intracellular Ca+ unlocking NMDA receptors -> increases expression of neuropeptides for plasticity -> central mediated pain
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27
Q

What is long term potentiation and how is it created?

A
  1. changes in the efficiency of the nervous system that could contribution to long term memory
  2. requires brief high frequency inputs to develop
  3. inputs can be mechanical or cognitive
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28
Q

How can you block the neurologic contributions to inflammation?

A
  1. blocking the non-MNDA (excitatory) and GABA-A (inhibitory) receptors at the DH of the spinal cord
  2. blocking the sympathetics does not help
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29
Q

What is the dorsal root reflex?

A

The neurologic chain of events responsible for central nervous system influence on peripheral inflammation

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30
Q

How does the dorsal root reflex for the neurologic contribution to inflammation work?

A
  1. acute depolarization of peripheral afferent in response to local inflammation
  2. peripheral afferent (PA) synapses on inhibitory non-NMDA and excitatory interneurons
  3. inhibitory non-NMDA release GABA into the synapse with the PA causing antidromic depolarization of the PA back to target tissue
  4. at target tissue PA release pro-inflammatory substances such as substance P and CGRP
  5. excitatory NMDA activate the spinothalamic tract
31
Q

What is complex regional pain syndrome?

A
  1. mechanism by which the sympathetic nervous system plays a role in maintaining a chronic state of pain
  2. sympathetic sprouts in the dorsal horn wrap around non-nociceptive cells bodies
32
Q

What are the signs and symptoms of complex regional pain syndrome?

A
  1. vasomotor and sudomotor changes
  2. abnormalities of hair and nail growth
  3. osteoporosis
  4. spontaneous burning
  5. hyperalgesia
  6. allodynia
33
Q

What is muscle stiffness?

A

its a ratio of muscle force change to muscle length created by intrinsic and extrinsic factor

34
Q

What are the intrinsic and extrinsic factor of muscle stiffness?

A
  1. intrinsic-connective tissues and actin/myosin interaction

2. extrinsic-reflex mediated tension by the muscle spindle

35
Q

How does muscle guarding become a positive feed back loop?

A
  1. initial injury and depolarization of type IV leads to gamma motor activation
  2. gamma motor leads to muscle guarding
  3. guarded muscles produce lactic acid and Potassium chloride
  4. which promotes greater type IV depolarization
36
Q

Why does the gamma loop have a bilateral effect?

A

it effects the primary Alpha motor neuron and the contralateral secondary Alpha motor neuron

37
Q

How does chronic myofascial pain start?

A

1.evolution of chronic guarding and trigger points

38
Q

What neurologic effects has manipulation demonstrated?

A
  1. influenced postural reflexes

2. inhibits facilitated segments

39
Q

Can type I and II mechanorecptors effect muscle tone?

A
  1. Yes, via the gamma motor loop
40
Q

Ankle sprains have demonstrated an inhibiting effect on what muscle group?

A

Hip extensors

41
Q

How can you use cutaneous receptors to treat to improve muscle recruitment?

A
  1. via there influence on the gamma motor loop
  2. cutaneous receptors also provide some kinesthetic afferent
  3. taping or wraps can influence this pathway
42
Q

How can you use the gamma motor system to improve muscle recruitment?

A
  1. increase spindle sensitivity to improve muscular response via repetitive exercise
  2. target monosegmental muscles that have the greatest spindle density
43
Q

Muscles spindles have an influence on what muscles

A
  1. uptrains agonist alpha motors
  2. down trains antagonist
  3. uptrains contralateral agonist
  4. downtrains contralateral antagonist
44
Q

When the primary mechanorecoptor are damaged what other receptors can you use to treat the area?

A
  1. cutaneous receptors
  2. Gamma motor systme
  3. GTO
45
Q

How can you use GTO to up-train an injury?

A
  1. intramuscular connective tissues contain GTO
  2. works to inhibit the gamma motor loop
  3. facilitates the antagonist
46
Q

What is the ideal exercise progression for retraining muscles spindle activity?

A
  1. concentric away
  2. isometric to fix gained range to stimulate spindle without compromising stability
  3. eccentric with functional loading patterns into the gained ROM
47
Q

What clinical findings are suggestive of a facilitated segment?

A
  1. segmental distribution alpha motor guarding or inhibition
  2. segmental sympathetic activity such as sweating, skin texture or fibrosis, flare or blanching response to scratch
  3. changes in electrical skin skin resistence
  4. taut band
  5. decreased joint mobility
  6. facet tenderness
  7. visceral symptoms
48
Q

What is convergence

A

Concept that the involved segment acts a focal lens for the abnormal input from the somatic, visceral and cortical systems

49
Q

How can over use syndromes develop from faciliated segments?

A

The muscle and vascular tone is increased so the muscle is working harder with less blood

50
Q

How does increased sympathetic tone effect sense organs?

A
  1. it decreases their threshold for actuation

2. examples include spindles, tacile, taste, olfactory, carotid sinus, pacinian corpuscles, retina, cochlea

51
Q

What is somatization of pain?

A

the tendency to experience pain that is unaccounted for by objective findings

52
Q

What are the two basic components of pain and what clinical unique pathology reflects both?

A
  1. senory discrimination- perception and detection
  2. affective-cognitive- relationship between pain and mood, attention to memory, coping with pain and rationalizing pain
  3. the facilitated segment is a focal lens for all of this neural information
53
Q

what are some peripheral signs of increased sympathetic activity?

A
  1. reduce colateral circulation
  2. reduce bone growth
  3. reduced adipose tissue
  4. reducted activity of the reticuloendothelial system
  5. increased endocrine activity
  6. inhibited tissue regeneration
54
Q

How does the cortex relate to the DH

A

1.The periaqueductal gray matter an integration center for the cortex that is in communication with the DH

55
Q

How can peripheral nerves contribution to sensitization of the peripheral nervous system?

A
  1. pathological peripheral nerves can sensitize the side range dynamic interneurons on the DN
  2. Healthy peripheral nerves can begin to fire eptopically
  3. Denerveated interneurons in the DH can become reinnervated by nociceptive fibers
  4. dymlination of ischemic nerve fibers can lead to eptopic firing as sodium channels form along the axon
56
Q

What is neurogenic inflammation?

A

part or the inflammatory process that is solely mediated by the actions of the peripheral sensory neurton

57
Q

What is the dorsal root ganglion?

A
  1. location of peripheral sensory nerve cell bodies

2. Contains A-beta, A-delta and C fibers

58
Q

What is the difference between A-beta, A-delta and C fibers?

A
  1. A-beta- mylenated, light touch and vibration, large diameter, rapid conduction, terminate deeper lamina III-IV
  2. A-delta- terminate lamina I and II respond to cold
  3. C fibers- terminate lamina I and II respond to heat
59
Q

What is the difference between a projection neuron and an interneuron

A
  1. projection- transfer info to and from the spinal cord to brain and help cortex manage the tone of the DH
  2. interneurons-short distance within spinal cord and either inhibit or excite
60
Q

How can the sympathetic nervous system contribute to central sensitization of pain?

A

you have have sympathetic sprouting in the DRG that can drive sensory tone

61
Q

What type of ion channels have NMDA receptors

A
  1. calcium
  2. potassium
  3. sodium
62
Q

What blocks NMDA receptors?

A
  1. magnesium

2. zinc

63
Q

What enzymes facilitates opening NMDA receptors?

A
  1. substance P

2. Nitric oxide enhance substance P release from neighboring terminals

64
Q

What role does nitric oxide play in the nervous system?

A
  1. it facilitates NMDA receptor opening and postsynaptic excitation
  2. it sis a natural biproduct following Ca+ channel opening
  3. diffuses to neighboring synapses increasing the release of substance P
65
Q

What is allostatsis?

A

the ability of the body to maintain stability through change via neuroendocrine, autonomic nervous system, and immune system

66
Q

How can the immune system effect pain?

A
  1. there is an infiltration of immune cells into the CNS with radiciopathy and neuropathy
  2. glial cells can sensitize the DRG
67
Q

Does pain perception require a mechanical input?

A

No, an emotional response is adequate

68
Q

What pattern does the development of neuropathic pain follow?

A
  1. normal-mechanically driven from the periphery
  2. faciliated- abnormal firing patterns (but there is a pattern) and no longer mediated by periphery
  3. neuropathic pain: no pattern and centrally mediated
69
Q

What is allostatic load and what are the signs of it being too high?

A
  1. measure of the negative effect on allostatis
  2. increased respiratory rate and HR
  3. decreased immune response and GI function
  4. behavioral changes
  5. melancholic depression
  6. repression of libido
  7. physiologic changes of CNS such as destruction of inhibitory neuron
70
Q

What are some symptomes of a low allostatic load?

A
  1. inflammatory response
  2. increaed interlukin 1 and 6
  3. hyperactive immune response with autoimmune disorders
  4. behavioral changes
  5. atypical depression (worthlessness, lethargic, hopeless, low anxiety)
  6. physiologic changes in CNS
71
Q

What is the really long word Rick likes to use and what is it?

A

cellulotenoperiosteomyalgia

  1. segmental dysfunction altering the sensitivity and texture of soft tissue
  2. dectectable by carful palpation of the the cutaneous, muscular and enthesis
72
Q

What are neurodynamics?

A

the mechanical and physiological properties of the peripheral nervous system that are dynamically interdependent and correlate the effects of tension and excursion on the peripheral nervous system

73
Q

What will happen if there are changes in neurodynamics?

A

you will develop adverse neural tension and mobility that can result in symptomalogy

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