21 - Neuropathic Pain Flashcards
Presentation and diagnosis of neuropathic pain
- 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)
What determines tx choice for neuropathic pain?
- 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
Opioids for PDN
- 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
Harms of TCAs for neuropathic pain **know this
- Notable SE (~10-30%) = anticholinergic, weight gain, sedation, orthostatic hypotension
- Cautions = elderly, dementia, glaucoma, urinary retention, cardiac disease
- Nortriptyline has fewer SE
Harms of gabapentin and pregabalin for neuropathic pain **know this
- 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
Harms of SNRIs for neuropathic pain **know this
- Notable SE = nausea (particularly for venlafaxine), increased BP, dizziness
- Cautions = HTN, bipolar disorder
Harms of tramadol for neuropathic pain **know this
- Notable SE = nausea, constipation, sedation, dizziness
- Cautions = opioid dependence/addiction risk, seizure risk
Non-pharms for neuropathic pain
- 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?
Neuropathic pain meds – specifics
- 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
Dosing of pain meds for neuropathic pain
- 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
Common comorbidities w/ neuropathic pain and possible drugs for both conditions
- *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?
What should be monitored for neuropathic pain? **know this
- Efficacy -> pain level, functioning (mobility, exercise tolerance, sleep, socialization, psychological status)
- Safety (SE) **also includes driving & fall risk
When should you monitor for neuropathic pain? **know this
Depends on rate of titration desired and self-management abilities of pt
Combination therapy for neuropathic pain
- 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
Topicals for neuropathic pain
- 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
Points for pt education for shared decision-making
- 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?
Cannabis overview and terminology
- 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
Indications for medical marijuana
- 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.
Components of cannabis (cannabinoids)
- 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
Commercial cannabinoids
- 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
Who would be a candidate for cannabis?
- 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
Physiological effects of cannabis
- 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
Cannabis use disorder – signs, sx of withdrawal, and tx
- 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