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PT 680 Clinical Medicine > Persistent and Neuropathic Pain Syndromes > Flashcards

Persistent and Neuropathic Pain Syndromes Flashcards

1
Q

what superficial receptors pick up the sensation of pain

A

nociceptors

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2
Q

on what afferents does fast, acute, well-localized pain travel to the spinal cord

A

A-delta

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3
Q

on what afferents does slow, chronic, dull, burning, aching, and poorly localized pain travel to the spinal cord

A

c-afferents

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4
Q

what are the two components of the anterolatearl spinothalamic tract that carry pain sensation to the thalamus

A

neospinothalamic
paleospinothalamic

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5
Q

what tract does fast pain travel

A

neospinothalamic tract

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6
Q

where does information from neospinothalamic tract go and what does it detect

A
  • goes to primary sensory cortex
  • detects location and intensity of pain sensation
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7
Q

what tract does slow pain travel

A

paleospinothalamic tract

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8
Q

where does information from paleospinothalamic tract go and what does it detect

A
  • goes to the reticular formation, amygdala, and cingulate gyrus
  • results in affective, motivational and autonomic responses to pain sensation
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9
Q

the ascending pain information on the ALS is transmitting what

A

a DANGER signal, NOT a pain signal itself

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10
Q

what is pain

A

a perception of danger signals

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11
Q

what 3 components make up the pain neuromatrix

A

cognition
body
emotion

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12
Q

describe the two ways in which pain can be modulated

A
  • closing the gate: perception of pain may be modulated by neurotransmitters released by interneurons in the spine by activation of the pain gate – application of heat, cold, massage, or TENS provides stimulus for local modulation
  • descending opioid pathways: central modulation of pain occurs when the descending opioid pathway is stimulated resulting in release of pain inhibiting neurotransmitters such as endorphins, enkephalins, beta-endorphins
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13
Q

associated with tissue damage, usually sudden and may be severe; produces a physiological response; should gradually disappear with removal of physical stimulus or as tissue heals

A

acute pain

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14
Q

persistent pain that adversely affects a pt’s well-being, function, or quality of life; associated with increased rates of depression, suicidal tendencies

A

chronic pain

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15
Q

how long does pain have to present for to be considered chronic pain

A

longer than 3-6 months –> which is past the expected tissue healing time

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16
Q

aberrant somatosensory processing in CNS/PNS; associated with peripheral neuropathies, SCI, post-stroke, MS, thalamic injury; presenting as shooting, burning pain, numbness, altered sensation

A

neuropathic pain

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17
Q

pain descriptors for muscle pain

A

cramping, dull, aching

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18
Q

pain descriptors for nerve root pain

A

sharp, shooting

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19
Q

pain descriptors for nerve pain

A

sharp, lightening-like, electric

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20
Q

pain descriptors for sympathetic nerve pain

A

burning, pressure, stinging, aching

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21
Q

pain descriptors for bone pain

A

deep, nagging, dull

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22
Q

pain descriptors for fracture

A

sharp, severe, intolerable

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23
Q

pain descriptors for vascular pain

A

throbbing, diffuse

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24
Q

receptors at site of injury become increasingly responsive or threshold for noxious stimulus decreases

A

peripheral sensitization

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25
Q

what is associated with peripheral sensitization

A

hyperalgesia

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26
Q

prolonged peripheral inflammation or inflammation in the CNS results in increased excitability in the dorsal horn and decreased inhibition via descending pathway

A

central sensitization

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27
Q

what is associated with central sensitization

28
Q

what should you screen for in patients with chronic pain

A

depression!!

29
Q

list common persistent pain conditions

A

arthritis (OA and RA)
headache/migraine
persistent neck/back pain/spinal stenosis
neuralgias
peripheral neuropathies
CRPS (SHS and RSD)
myofascial pain syndrome
fibromyalgia
cancer related pain
postoperative pain
thalamic pain syndrome
pain associated with stroke, MS, SCI

30
Q

what are the 3 types of headaches/headache syndromes

A

primary HA
secondary HA
cranial neuralgias and primary facial pain conditions

31
Q

what are the 4 types of primary HA

A

migraine
tension
trigeminal autonomic cephalgias (TCA)
other primary headache disorders

32
Q

caused by CNS excitability in nerve fibers within wall of brain blood vessels and also trigeminal N

33
Q

what is the most common type of HA

34
Q

usually self-managed but may become chronic if occurring more than 12 days/year

A

tension HA

35
Q

what causes tension HA

A

sensitization of peripheral nerves in pericranial myofascial areas

36
Q

what causes trigeminal autonomic cephalgias (TACs)

A

excessive stimulus of trigeminal complex

37
Q

how many types of trigeminal autonomic cephalgias are there and what is the most common

A

4
cluster headache

38
Q

rare but extremely painful, excruciating pain on one side of the head around/behind the eye; may be episodic or chronic; occurs in cycles across lifespan following circadian rhythms and seasonal changes; prevalent in men 20-40 y/o and occurs in early morning

A

trigeminal autonomic cephalgias

39
Q

occur as a result of an underlying pathology and would signal a red/orange flag

A

secondary HA

40
Q

examples of causes of secondary HA

A

subdural hematoma, subarchnoid hemorrhage, increased ICP secondary to TBI/concussion, meningitis, brain abscess, CNS conditions, cerebral neoplasms, toxicity, sinusitis, otitis media

41
Q

referred from cervical zygopophyseal joints or intervertebral discs in the neck and perceived as head/face pain

A

cerviogenic HA

42
Q

what nuclei are involved with cervicogenic HA

43
Q

signs and sx of cervicogenic HA overlap with

A

migraine without aura and tension-type HA

44
Q

s/s that are different from migraine with cerviogenic headache

A

reduced C/s PROM/AROM
may have arm pain
can reduce sx with palpation/motion

45
Q

what can be used to measure the impact of cerviogenic HA

A

NDI (neck disability index)

46
Q

irritation to CN V causing severe facial pain and spasms; sharp knife-like pain lasting < 2 minutes with multiple attacks a day; “lightning bolt” pain sensation; pain may follow distribution of N branches

A

trigeminal neuralgia (tic doulourex)

47
Q

what are the 3 branches of the trigeminal N

A

opthalamic
maxillary
mandibular

48
Q

causes of trigeminal neuralgia

A
  • N irritation due to contact of healthy artery/vein against trigeminal N (increased pressure causing abnormal firing; due to trauma increasing pressure; herpes zoster virus causing inflammation)
  • demyelination of CN 5 (MS)
  • many unknown causes
49
Q

how to diagnosis trigeminal neuralgia

A

neuro exam
MRI
no special tests - dx of exclusion

50
Q

triggers for trigeminal neuralgia

A

touching skin lightly
shaving
brushing teeth
blowing nose
drinking hot/cold beverages
applying makeup
smiling
talking

there are a lot of unknown triggers and can often have multiple triggers

51
Q

treatment trigeminal neuralgia

A
  • pharmalogical: anticonvulstants (carbamazepine, phenytoin); muscle relaxant (balcofen); gabapentin (anticonvulsand but used for neuropathy/pain)
  • surgical: microvascular decompression, percutaneous sterotactic rhizotomy, percutaneous balloon compression; stereotactic radiosurgery
  • PT: education, biofeedback to help reduce pain, relaxation techniques, neurodynamics, r/o other causes (TMJ, HA, dental issues)
52
Q

when can peripheral neuropathy occur

A

when there is disease or injury to somatic, cranial or autonomic nerves

53
Q

when does central neuropathy occur

A

after stroke, spinal cord injury, in MS or other CNS disorder

54
Q

how is neuropathic pain described

A

shooting, burning, numbness, alterations in sensation and paresthesia that are often hard to describe

55
Q

what are some risk factors of developing persistent pain conditions

A
  • genetic factors for central sensitization
  • comorbid conditions (migraine, fibromyalgia, CRPS, persistent LBP, IBS, chronic tension HA, TMJ disorder, depression, pain disorder, PTSD, pelvic pain, TN)
  • W > M
  • psychosocial h/o trauma, abuse, stress, poor coping skills
  • lack of social support, limited access to preventative care
  • stress
  • smoking, alcohol and drunk addiction, obesity/overweight
  • nutritional contributions from lack of vitamin D and b-vitamin
56
Q

what is a specific scale that can be used for neuropathic pain

A

Leads Assessment of Neuropathic Symptoms and Signs
LANSS

57
Q

how to diagnose persistent pain conditions

A

no specific imaging/lab tests
dx by exclusion

58
Q

OTC for persistent pain conditions

A

acetaminophen

59
Q

NSAIDs for persistent pain conditions

A

naproxen, ibuprofen

60
Q

topical for persistent pain conditions

A

capsaicin, lidocaine, salsalate, menthol

61
Q

antidepressants for persistent pain conditions

A

amitriphyline, tricyclics

62
Q

anticonvulsants for persistent pain conditions

A

gabapentin, cyclobenzaprine

63
Q

muscle relaxants for persistent pain conditions

A

balcofen, cyclobenzaprine

64
Q

weak opiates for persistent pain conditions

65
Q

strong opiates for persistent pain conditions

A

codeine, hydrocodone, morpine, fentanyl patch

66
Q

general principles for persistent pain management

A
  • improve ability to cope with pain
  • teach non-pharmalocigal management techniques
  • increase physical strength, endurance, mobility, independence
  • improve sleep
  • teach proper body mechanics
  • increase social, recreational activities
  • enhance vocational opportunities
  • teach why they are having pain
67
Q

PT interventions for persistent pain

A
  • graded exercise, aerobic conditioning, functional-based activities
  • manual therapy (soft tissue, trigger point)
  • neuromuscular reeducation (EMG biofeedback, diaphragmatic breathing, PNF)
  • AD
  • physical agents
  • complementary approaches (yoga, tia chi, acupuncture, dry needling, mind-body therapies)
  • pain education

PT 680 Clinical Medicine (18 decks)

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