21 - Neuropathic Pain Flashcards

1
Q

Presentation and diagnosis of neuropathic pain

A
  • Pain reported often not evident by physical assessment
  • Common descriptors = shooting, burning, electric shock, pins and needles, allodynia, hyperalgesia
  • DN4 questionnaire most common
    • If score 4 or greater, test is positive (83% sensitivity, 90% specificity)
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2
Q

What determines tx choice for neuropathic pain?

A
  • Efficacy (little efficacy data)
    • Greatest evidence for painful diabetic neuropathy (PDN) and post-herpetic neuralgia b/c more common so more research is done
  • Px goals
    • What function means to the pt and degree of change
  • Desire for specific harm avoidance
  • Comorbidities
  • Feasibility
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3
Q

Opioids for PDN

A
  • Very low-quality evidence proving value in tx
  • Overall not used b/c potential for dependence and abuse
  • Tramadol
    • MOA = weak m-opioid receptor agonist activity and inhibition of NE/5-HT reuptake
    • Although has a lower potential for abuse compared w/ other opioids, given the safety concerns it isn’t recommended as 1st or 2nd line agent
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4
Q

Harms of TCAs for neuropathic pain **know this

A
  • Notable SE (~10-30%) = anticholinergic, weight gain, sedation, orthostatic hypotension
  • Cautions = elderly, dementia, glaucoma, urinary retention, cardiac disease
  • Nortriptyline has fewer SE
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5
Q

Harms of gabapentin and pregabalin for neuropathic pain **know this

A
  • Notable SE = dizziness, sedation, peripheral edema (don’t want to treat this w/ a diuretic; often have to switch if edema becomes bothersome)
  • Cautions = elderly, existing edema, fall risk, abuse potential
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6
Q

Harms of SNRIs for neuropathic pain **know this

A
  • Notable SE = nausea (particularly for venlafaxine), increased BP, dizziness
  • Cautions = HTN, bipolar disorder
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7
Q

Harms of tramadol for neuropathic pain **know this

A
  • Notable SE = nausea, constipation, sedation, dizziness

- Cautions = opioid dependence/addiction risk, seizure risk

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8
Q

Non-pharms for neuropathic pain

A
  • Behavioural, psychosocial, physical and other therapies are essential for long-term management
  • Interdisciplinary intervention may decrease drug requirements
  • Exercise, relaxation, CBT, music therapy
  • Overall DM2 benefit and decreased CV risk
  • Decreased neuropathic sx?
  • Muscle strengthening & balance to reduce falls?
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9
Q

Neuropathic pain meds – specifics

A
  • Most drugs require a trial of 2-4 weeks; usually try 4 weeks
  • *Let px know this is a slow process
  • Fast track = increase dose by 50-100% q3days
  • Cautious = increase dose by 50-100% q1week
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10
Q

Dosing of pain meds for neuropathic pain

A
  • Always start low and go slow (this is a chronic condition and not worth risking harm to the pt)
  • SE may result in a loss of a viable option in the mind of the pt
  • Higher doses have a low likelihood of resulting in greater benefit and are more likely to result in greater harm
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11
Q

Common comorbidities w/ neuropathic pain and possible drugs for both conditions

A
  • *If someone is stable on a drug for one condition, never switch just because it might help w/ another condition; only use this when starting new meds
  • Depression/anxiety -> SNRI, TCA?
  • Insomnia -> TCA, gabapentin?
  • Osteoarthritis -> duloxetine, tramadol?
  • Migraine -> TCA
  • Most other types of neuropathic pain -> SNRI, TCA, gabapentin, pregabalin, tramadol?
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12
Q

What should be monitored for neuropathic pain? **know this

A
  • Efficacy -> pain level, functioning (mobility, exercise tolerance, sleep, socialization, psychological status)
  • Safety (SE) **also includes driving & fall risk
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13
Q

When should you monitor for neuropathic pain? **know this

A

Depends on rate of titration desired and self-management abilities of pt

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14
Q

Combination therapy for neuropathic pain

A
  • Studies generally small w/ some questionable methodology
  • Some combos w/ some positive data:
    • Gabapentin + nortriptyline
    • Gabapentin + opioid -> for the study, NNT = NNH plus concerns w/ long-term opioid use
    • Topical amitriptyline + ketamine
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15
Q

Topicals for neuropathic pain

A
  • Lidocaine
    • 5% plaster or patch most studied -> modest benefit in low quality, short-term trials
    • 1st or 2nd line in several guidelines for PHN
    • Advantage -> immediate onset and minimal systemic absorption
  • Capsaicin
    • 0.075% gel showed insufficient data to draw conclusions
    • 8% patch showed benefit but not available in Canada
  • Ketamine alone -> case series supporting pain relief vs. placebo
  • Amitriptyline + ketamine
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16
Q

Points for pt education for shared decision-making

A
  • Likelihood of benefit
  • When to likely see a reliable benefit
  • SE (what are they and how common are they; talk about what to do if they happen)
  • Approx. cost
  • If several reasonable options to choose from, which would the pt prefer based on these?
17
Q

Cannabis overview and terminology

A
  • Cannabis = preferred term instead of marijuana; sativa, indica, and ruderalis
    • Used recreationally for euphoric effects; primary psychoactive component is THC
    • May use “recreational” cannabis for medicinal purposes (who is counselling them?)
    • Medicinal use based on recommendation/Rx by an appropriate HCP for a known medical condition that has evidence for efficacy
  • Cannabinoids: chemical compounds that are active at cannabinoid receptors in the body; can be plant sourced or synthetic
18
Q

Indications for medical marijuana

A
  • On-label = pain (cancer-related, neuropathic), MS-related spasticity, chemotherapy-induced N/V, anorexia (HIV/AIDS)
  • Off-label = RA, spinal cord injury, epilepsy, insomnia, anxiety, etc.
19
Q

Components of cannabis (cannabinoids)

A
  • THC – principal psychoactive component
    • Increases pleasure, appetite
    • Decreases memory, cognition
  • *Analgesia
  • Cannabidiol (CBD) = no psychoactivity
    • Antiemetic, antispasmodic properties
    • Analgesia, anti-inflammatory
    • Anti-anxiety
  • Cannabinol (CBN) = mild psychoactivity
    • Anti-inflammatory
    • Immunosuppressive effects
20
Q

Commercial cannabinoids

A
  • Nabilone -> oral capsule, semi-synthetic analogue of THC; chemotherapy induced N/V; AE = dizziness, drowsiness, dry mouth
  • Sativex -> oromucosal spray containing THC and CBD; doesn’t produce a significant “high” unless at very high spray use; used for spasticity in MS
  • *Generally preferred over cannabis due to safety and dosing predictability
21
Q

Who would be a candidate for cannabis?

A
  • Not typically 1st or 2nd line therapy for any indication
  • Reserve use for px who have failed 3 or more other therapies for neuropathic pain
  • Relative CI = age < 21-25, hx of psychosis/ schizophrenia, or substance abuse hx
    • Doesn’t cause schizophrenia if you aren’t predisposed; can precipitate first episode sooner and can precipitate psychotic events
  • Like opioids, should be prescribed as a trial and have an exit strategy in place
22
Q

Physiological effects of cannabis

A
  • Timing depends on route (acute can begin w/in 30 seconds & last 4-12 hours)
  • Acute -> memory impairment, motor coordination effects, psychosis, increased HR, increased risk of MI w/in 60 mins after smoking due to increased cardiac demand (caution w/ MI hx or those w/ other cardiac conditions), orthostatic hypotension, analgesia
  • Chronic -> dependence, bronchitis/emphysema, increased risk of psychotic disorders, poor learning and memory recall
    • Adolescents (< 25 y/o) -> altered brain dev’t, cognitive impairment, poor educational outcomes
23
Q

Cannabis use disorder – signs, sx of withdrawal, and tx

A
  • Signs of CUD during tx:
    • Wanting high potency THC only
    • Misuse of other substances
    • Poor functioning
    • Rapid or unsanctioned dose increased
    • Missed follow-up; reports of lost or stolen cannabis
  • Sx of cannabis withdrawal (onset 1-2 days, peak 2-6 days) -> anger, aggression, appetite change, weight loss, anxiety, irritability
  • Treating CUD -> brief interventions, withdrawal management, and psychosocial interventions