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PHTY2101 EOS > B2 L23 Part 2 Neuropathic Pains > Flashcards

B2 L23 Part 2 Neuropathic Pains Flashcards

1
Q

What is neuropathic pain?

A

Pain caused by a lesion or disease of the somatosensory nervous system (Neuropathic pain is a clinical description and not a diagnosis.

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2
Q

What is central neuropathic pain?

A

with a lesion (e.g. imaging, neurophysiology, biopsies, lab tests) or disease (e.g. stroke or genetic abnormality) of the central somatosensory nervous system

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3
Q

What is peripheral neuropathic pain?

A

with a lesion/disease of the peripheral somatosensory nervous system.

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4
Q

Although commonly a cause of chronic symptoms, neuropathic pain can also present acutely following _____ and _____. The incidence has been conservatively estimated as 3% of acute pain patients and often it produces ______ symptoms.

A

trauma; surgery; persistent

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5
Q

What is nociplastic pain?

A

Pain that arises from altered nociception, despite no clear evidence of actual or threatened tissue damage causing theactivation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system (includes central nervous system) causing the pain. Unknown lesion

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6
Q

Neuropathic pain can develop after injury to ______along ____ and ______ modulatory pathways in the central nervous system.

A

neurons; nociceptive; descending

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7
Q

Neuropathic pain also plays a part in other ______ disorders, with high comorbidity for ____ pain, sleep disorders, and psychological conditions such as depression. Drugs that _____ (are/are not) effective for one condition may benefit others.

A

neurobiological; chronic; are

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8
Q

Neuropathetic pain has a _____ (high/low) impact on person, _____ (high/low) cost to system and difficult to identify precise targets for intervention. Can be described as a disease process or a syndrome.

A

high; high

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9
Q

What is the main difference between nociceptive vs neuropathic/nociplastic pain?

A
  • Nociceptive pain is expected
  • Nociceptive pain (including inflammation as a stimulus, and originating from somatic or visceral regions) contributes important warning information, to drive change in behaviour to protect the affected region from further injury and for healing to occur
  • Neuropathic / Nociplastic pain does not serve any useful biological function.
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10
Q

Nociceptive pain (including inflammation as a stimulus, and originating from somatic or visceral regions) contributes important _________, to drive change in behaviour to protect the affected region from further injury and for healing to occur

A

warning information

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11
Q

Neuropathic / Nociplastic pain does not serve any useful _____ function.

A

biological

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12
Q

What are 2 factors that non-neuropathetic pain is distinguished?

A
  1. There is no transduction (conversion of a nociceptive stimulus into an electrical impulse).
  2. Prognosis is poor: injury to major nerves is more likely than injury to non-nervous tissue to result in chronic pain.

Neuropathic pain tends to be refractory to conventional analgesics (non-responsive, persistent & moderate-high intensity) than non-neuropathic pain.

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13
Q

Neuropathic pain tends to be ____ to conventional analgesics (non-responsive, persistent & moderate-high intensity) than non-neuropathic pain.

A

refractory

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14
Q

The requirement for “nerve injury” in neuropathic pain is _____.

A

contentious i.e. elimination of other causes, and one of them is uncertain

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15
Q

How does neuropathic pain present in the patient interview/exam for mechanism of injury?

A

could be a clear mechanical stress to nervous system, or could be little or no threat to tissues.

With either mechanism, symptoms persist months or years beyond initial injury.

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16
Q

How does neuropathic pain present in the patient interview/exam for pain area?

A

may be discrete or general e.g. peripheral nerve path or body region

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17
Q

How does neuropathic pain present in the patient interview/exam for pain quality?

A

often described as stabbing, shooting, electric-shock or nerve-like pain. Input vs ouput perception suggests hyperalgesia or allodynia

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18
Q

How does neuropathic pain present in the patient interview/exam for neurological deficits?

A
  • Sensory deficits or paresthesia
    • e.g. tingling, pricking or pins & needles.
  • Motor deficits may also be present.
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19
Q

How does neuropathic pain present in the patient interview/exam for autonomic signs?

A

changes in colour, temp, swelling, sweating observed in 30-50% of cases

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20
Q

How does neuropathic pain present in the patient interview/exam for aggravating factors?

A

could be situational (memory) with or without mechanical stress, summative or unpredictable. Consider if pain persists or worsens when tissues not loaded e.g. 3am.

21
Q

What are 2 things that allodynia can include?

A
  1. Ectopic discharges
  2. Abnormal impulse generating sites (AIGS)
22
Q

What is ectopic discharge?

A

at the peripheral terminal, associated with damage to a nerve, aberrant repair process and/or the chemical environment of the neuron

23
Q

What is a Abnormal impulse generating sites (AIGS)?

A

regions of ectopic firing associated with demyelination of a neuron

24
Q

What is 1 thing that secondary hyperalgesia can include?

A

Expansion of receptive field

25
Q

What is expansion of receptive field?

A

Neurones are able to achieve action potential threshold with stimulus to a larger superficial region.

26
Q

What are 4 things that allodynia and hyperalgesia can include?

A
  1. Up or down regulation of sodium channels
  2. Ephaptic transmission
  3. Disinhibition at the spinal cord
  4. Descending pathways: from supraspinal structures such as the periaqueductal gray matter
27
Q

What occurs during up or down regulation of sodium channels?

A

e.g. in cells of the DRG or at the site of a nerve injury where a neuroma forms.

28
Q

What occurs during ephaptic transmission?

A

ectopic firing of neurones close to (but not synapsing) with another that is firing. Like electrical “cross-talk”.

29
Q

What occurs during disinhibition at the spinal cord?

A

downregulation of normal inhibitory mechanisms at the spinal cord may be clinically evident if hyperalgesia relates more to mechanical stimuli than thermal.

  • The balance between inhibition and amplification is dynamic and influenced by context, behavior, emotions, expectations, timing, and pathology
30
Q

What occurs during descending pathways: from supraspinal structures such as the periaqueductal gray matter?

A

modulate transmission of nociceptive signals in the spinal cord.

31
Q

What is 5 and how is it associated with neuropathic pain?

A

Anterior cingulate cortex: anxiety, anticipation of pain, attention to pain, and motor responses

32
Q

What is 3 (into gyrus) and how is it associated with neuropathic pain?

A

Insular cortex: sensory discriminative and affective aspects of pain that contribute to the negative emotional responses and behaviors

33
Q

What is 7 and how is it associated with neuropathic pain?

A

Prefrontal cortex: sensory integration, decision making, memory retrieval, and attention processing in relation to pain

34
Q

What is 4 and how is it associated with neuropathic pain?

A

Primary and secondary somatosensory cortices: localize and interpret noxious stimuli

35
Q

What is 9 (deep) and how is it associated with neuropathic pain?

A

Nucleus accumbens: which is involved in placebo analgesia

36
Q

What is 6 (deep) and how is it associated with neuropathic pain?

A

Amygdala & 2: Hippocampus and other parts of the limbic system: formation and storage of memories associated with emotional events, affect, arousal, fear that accompanies pain and attention to pain and learning

37
Q

Daily stressors and the stress-vulnerability factor ‘worrying’ predict the short-term course of RA _____, ______ and ______. Specific cytokines predict short-term fluctuations of fatigue.

A

disease activity; fatigue; pain

38
Q

What are some common associated features of chronic widespread MSK pain?

A

Fatigue with non-restorative sleep pattern, irritable bowel, headache, subjective swelling, psychological distress/depression, functional disability.

39
Q

What are some possible mechanisms of chronic widespread MSK pain?

A
  • Imbalance in neurotransmitters: Substance P and serotonin
  • Impaired Hypothalamus-Pituitary-Adrenal (HPA) axis for stress responses of the neuro-endocrine system.
  • Impaired C fibre functions: less regeneration, increased threshold for temperature
40
Q

What are some pharmacological RX of chronic widespread MSK pain?

A

Antidepressants, antiepileptics and serotonin/norepinephrine modulators.

41
Q

What is conservative treatment of chronic widespread MSK pain? List 4 treatments.

A
  1. Education
  2. Exercise
  3. Biofeedback
  4. Relaxation
42
Q

What did quantitative sensory testing show in testing of fibromyalgia?

A

showed that patients with fibromyalgia had increased detection thresholds for cold and heat (i.e. colder cold and hotter hot in order to detect) as evidence of impaired small fibre function (C fibres).

43
Q

What did dermal nerve fibre density ( and regenerating intra-epidermal nerve fibres in skin punch biopsies of the lower leg and upper thigh) show in testing of fibromyalgia?

A

Showed that it was only the small unmyelinated (C fibres) that had lower rates of regeneration and fibre bundles

44
Q

What is Complex Regional Pain Syndrome?

A

Multiple biological pathways underlie the clinical features of CRPS, such as aberrant inflammation, vasomotor dysfunction, and maladaptive neuroplasticity.

  • Bad response to tissue injury.
  • Immobilisation leads to CRPS. Remobilisation resolves CRPS
45
Q

On Whiplash Associated Disorders without fracture (WAD II), what did the NDI reveal?

A

The neck pain and disability index (NDI) revealed no differences in frequency of recovery between pragmatic and usual care groups at 6 months, indicating no advantage of the early multiprofessional intervention.

46
Q

What are the 4 sympathetic nervous system symptoms of Complex Regional Pain Syndrome? What are 2 ways the symptoms can be aggravated?

A
  • changes in (at the affected region)
    1. temperature
    2. colour
    3. sweating
    4. swelling
  • aggravation of symptoms by:
    1. cold exposure
    2. stress (e.g. fight-or-flight response).
47
Q

What are the 4 mechanisms of injury for a Whiplash Associated Disorder without Fracture (WAD II)?

A
  1. Lesions of Z joints or other places.
  2. Augmented central nociceptive processing: global cold hyperalgesia
  3. Stress system responses
  4. Psychosocial and sociocultural factors
48
Q

WAD II people get _______infiltrates in neck muscles.

A

fatty

49
Q

What is the treatment of WAD II?

A

No advantage of early multi-professional intervention.

PHTY2101 EOS (22 decks)

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