1 adequate therapy for chronic non cancer pain
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Adequate therapy for chronic non-cancer pain:
Current barriers and thoughts for the future
Dr. Yoram Shir
Alan Edwards Pain Management Unit
McGill University Health Centre
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Disclosure
The speaker cannot identify any potential conflict of
interest and has no relationships that should be
disclosed
Objectives
To review the prevalence of chronic non-cancer pain (CNCP)
To review specific therapeutic approaches To recognize the barriers for better treatment To suggest changes in our approach to CNCP
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Pain
“An unpleasant sensory and emotional
experience associated with actual or potential
tissue damage or described in terms of such
damage” (IASP)
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The gate control theory
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Brain
Peripheral nociceptors
Pain pathways
Spinal cord
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Types of pain
Acute vs. chronic Malignant vs. benign
Physiological vs. pathological Nociceptive vs. visceral Neuropathic Idiopathic
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Acute vs. Chronic Pain
Acute Symptom Short-term Warning sign Anxiety Responds well Single treatment
Chronic Disease Long-term False alarm Depression Less likely to respond Multidisciplinary approach
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Non malignant vs. malignant pain
”…we have deliberately not used the term ‘non-malignant pain’ because unrelieved chronic pain associated with any disease is indeed malignant” (Gourlay et al, 1991)
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Definition: chronic non-cancer pain
“…pain that has been present for at least six months or that has persisted longer than the expected time for tissue healing or resolution of the underlying disease process.” [Canadian Pain Society Guidelines, 2002]
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Prevalence of chronic pain
> 80% of cancer patients 10-40% of the general population > 50% following some surgeries ~ 25% in hospitalized populations 45-80% of the elderly populations 25% in Canada
Pain in the elderly
In the USA, 17% of the population is 60 years or older
More than 38 million individuals in the USA are 65 years or older
By 2030 the number of persons aged 65 years or older in the USA will increase to an estimated 71 million
By 2025, 1.2 billion people worldwide will be aged 60 years or older
Prevalence of chronic pain in elderly people
Difference between community dwelling people & long term care
Prevalence 3.7%-80% 80% of old people with cancer Could be due to central degenerative changes,
muscle weakness & slower rate of tissue healing
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Burden of chronic pain
Became a global disease Worldwide crisis In the USA alone:
Half million lost workdays/annum Healthcare costs > $150 billion/annum Steady increase in cost (e.g., 70% 1988-1995)
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Chronic pain in Canada
2/3 of Canadian primary care practitioners believe that moderate/severe chronic pain is not well managed
Median waiting time for 1st appointment in multi-disciplinary pain centers in Canada is 6 months (2-14 months)
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The chronic pain spiral
PainPainCenteredCentered
LifeLife
WEAK TIGHT
MUSCLES
LIMITS ACTIVITIES DECONDITIONING
HURT VS. HARM
PERSISTING PAIN
TISSUE DAMAGE
INJURYILLNESS
SURGERY
STIGMA
LOSS OF CONTROL
DECREASED PHYSICAL &
SOCIAL FUNCTIONING
DEPRESSION
Jovey RD. Pain focus. 2007;1.
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Pain assessment tools
Pain measurement
Pain History
Psychosocial history (mood, substance abuse,
functional level, family, occupation, etc.)
Goals & expectations
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Interpreting changes in pain intensity
Decrease in pain intensity
Clinical significance
10 – 20 % Minimal
≥ 30% Moderate
≥ 50% Substantial
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Barriers to effective pain management
The physician: Believing patients always tell when having pain Lack of training/knowledge Fear of regulatory scrutiny Concerns about addiction and side effects Time consuming Pain management is secondary to disease management Believing pain is a symptom, not a disease Failure to define goals and expectations
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Goals
PALLIATION REHABILITATION
SIDE EFFECTSCOST
AVAILABILITYCLINICAL EXPERTISE
Optimize balance between analgesia and adverse effects
ANALGESIA ADVERSE EFFECTS
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Barriers to effective pain management
The patient: Misconception that pain is normal Unwillingness to report pain Fear of side effects and addiction Believing that therapy may prevent control of more
severe pain in the future Cognitive impairment in elderly Depression Passive coping strategies
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Barriers to effective pain management
The system: Lack of resources Wrongful use/investments of the existing limited
resources Lack of basic education Permissive compensatory system
The reality of CNCP
Once developed, our ability to effectively treat CNCP is restricted
Nevertheless, most traditional basic research efforts & clinical pain-relieving approaches focus on pain palliation rather than prevention
Palliative therapeutic modalities
• Non-pharmacological approaches• Analgesic medications
• Invasive interventions
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WHO analgesic ladder
I IIIII
Pain Intensity
non-opioids + adjuvants
weak-opioids + non-opioids+ adjuvants
strong-opioids +non-opioids
+ adjuvants
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Analgesic ladder: multimodal modification
I II III
Pain Intensity
non-opioids +non-invasive
measures
opioids +non-invasive
+simple invasive measures
opioids +non-invasive +super invasive
measures
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Non-pharmacological measures
Psychological & behavioral therapy
CAM & diet
Relaxation, biofeedback, hypnosis
Physical modalities
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Invasive measures
Trigger point injections
Nerve blocks
IV lidocaine/ketamin/bisphosphenates infusions
Spinal axis interventions
Sympathectomy
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Super -invasive measures
Peripheral nerve, spinal cord & brain stimulation
Implanted spinal pump
Ablative surgery
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Pharmacological modalities
Non-opioid analgesics Opioids Adjuvants Marijuana and marijuana derivates
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Non-opioid analgesics – tramadol
Centrally acting synthetic non-opioid structurally related
to codeine Tramadol/morphine potency ratio: 1:4 2 enantiomers:
(-) Tramadol – weak mu agonist (+) Tramadol - inhibits serotonin reuptake
Up to 95% oral bioavailability
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Dose recommendation
Tramadol/acetaminophen: 1-2 Tb. Every 4-6h Tramadol extended release: once daily, not
beyond 400mg Reduced dose in kidney disease
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Clinical aspects Effective in nociceptive, neuropathic & mixed pain conditions Abuse potential:
Probably less than opioids Similar to NSAID
Side effects: Serotonin syndrome Similar to opioids: dizziness, nausea, vomiting, sweating < opioids: constipation, sedation
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Nucynta
Centrally acting analgesic Dual action: μ-opioid agonist & NA reuptake
inhibitor. Potency between tramadol and morphine in
effectiveness Immediate and extended -release preparations 50mg Tb., up to 250mg/daily
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Adjuvant analgesics
Mood stabilizers & antidepressants Sleep promoters Anti - epileptics Marijuana derivates Steroids
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Antidepressants:Tricyclics - amitriptyline
Suggested mechanism: CA reuptake inhibitors
Affinity for opioid receptors NMDS blockers Voltage-gated Na(+) channels blockers
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Amitriptyline
Clinically effective in: Postherpetic neuralgia Diabetic neuropathy Tension type headache Central pain due to stroke Fibromyalgia
Common anti-cholinergic side effects Suggested dose: 10 (5) – 75mg
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Noradrenergic/serotonergic
antidepressant Could possess direct analgesic properties:
Mirtazapine (remoron) - tension-type headache Bupropion (welbutrin) - neuropathic pain Venlafaxine (effexor) – Visceral & neuropathic pain Duloxetine (cymbalta) – diabetic peripheral neuropathy,
fibromyalgia , non-radicular LBP
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Anticonvulsants
Commonly used in chronic pain Possible analgesic mechanisms:
increasing GABA inhibition modulating sodium and calcium channels inhibiting excitatory amino acids decreasing abnormal neuronal hyperexcitability
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Carbamazepine
Traditionally regarded as the gold-standard Effective in trigeminal neuralgia & diabetic neuropathy Side effect profile opened the way for gabapentin No clinical studies comparing it to gabapentin &
pregabalin
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Gabapentin Acts through increased synaptic GABA
& calcium blockade at the CNS Proven effects:
Post traumatic neuropathic pain Peripheral neuropathy PHN Preemptive analgesia for PO pain Neuropathic pain due to cancer
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Gabapentin – in what dose?
Effective dose: 900-1,800mg/day Dose range seen at the clinic: 100-9,600mg/day Suggested dose:
Start with 100mg T.I.D. Stop at 2,800/day
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Gabapentin – side effects
Common: Somnolence Dizziness Ataxia, nervousness & tremor
Be aware of: Joint & diffused body pain Peripheral edema Tolerance?
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Pregabalin Beneficial in:
PO pain Diabetic peripheral neuropathy PHN Fibromyalgia
Recommended dose: 75-600mg/day Almost as popular as Tylenol among chronic pain patients Mostly used in Quebec off-label
Cannabinoids
Anonymous cross-sectional survey of 209 Canadians with
chronic pain1:35% reported using cannabis15% reported using cannabis for pain relief Mainly young people, post trauma/surgeryA wide range of amounts and frequency of cannabis usePain, sleep & mood were all subjectively improved
1Ware MA et al, Pain 102;211-6:2003
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Cannabinoids Oral synthetic preparations:
Nabilone (Cesamet): 0.5-4mg/day
Dronabinol (Marinol): 2.5-10mg/day
Sativex: cannabis-based buccal spray (neuropathic pain)
Indications: - 2nd line adjuvant pain therapy
- Insomnia
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Switching from pathogenetic treatment with alpha-lipoic acid to gabapentin and other analgesics in
painful diabetic neuropathy: a real-world study in outpatients1
1Ruessmann HJ et al, J Diabetes Complications 23;174:2009
Chronic pain palliation – Does it work?
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443 chronic DM patients treated with lipoic acid (600mg/d) for a mean period of 5 years
Switched to gabapentin (600-2400mg/d) or D/C therapy In the untreated group 73% developed pain within 2 weeks In the gabapentin group:
45% developed side effects and stopped treatment 55% of patients tolerating gabapentin did not respond to a
dose of 2400mg/g
Investments in pain palliation1
1Chappell AS, et al, Pain 146;253-60:2009
1Bansal D et al, Diabetic Medicine 26;1019-26:2009
Outcome of chronic pain therapy
4-year community study1: Increased prevalence (45.5 to 53.8%) 79% still reported pain after 4 years
Retrospective study of patients with CRPS2: None had recovered In most- only modest symptom improvement Improvement not necessarily associated with
therapy
1Elliott AM et al, Pain 99;299-307:2002; 2Schwartzman RJ et al, Clin J Pain 25;273-80:2009
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Limitations of injection therapy for LBP
LBP will be experienced by most humans during their life
1/5 will consult her/his GP Specific diagnosis is lacking in ~ 85% The scientific evidence for many of the
interventions is lacking
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Outcome of injection therapy
Epidural steroids injection: Short term relief: NNT of 7 Long term relief: NNT of 13 The best study to date – no short or long-term
effect
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Outcome of injection therapy
Facet joint injections: Not effective
Trigger point injections: Hardly effective
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Multiple reviews of injection outcome in patients with LBP lasting for more than 1 month:
Treatment with facet, epidural or local injections was not beneficial immediately or late after the intervention
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Summary – therapies for chronic pain
The prognosis of chronic pain is frequently poor despite advanced knowledge and novel therapeutic tools
Most resources are invested in palliation and not prevention
We, therefore, could focus more on: Prevention The environment Complementary & alternative medicine (CAM)
A call for change – prevention rather than palliation
Learn from other major diseases like cancer: 1971: President Nixon declares ‘War on Cancer’1
Cancer Act approved by Congress Massive funding of cancer therapy but not cancer
prevention Cancer mortality has not decreased as expected
(10% in 2005, lower than the expected 50%)
1Sporn MB, Lancet 347;1377–81:1996
The cancer model – palliation vs. prevention
While treatment is effective for certain cancers, it ranks behind both early detection and risk-factor modification in its potential to reduce cancer mortality1
Calls to view cancer not only as a curable illness but primarily a preventable one2
1Danaei G et al, Lancet 366;1784 –93:2005; 2Bailar JC 3rd et al, N Engl J Med 336;1569–74 :1997
Preventing CNCP
Identify patients at risk
Environmental contribution
Prevention of CNCP
Preventive analgesia; Multimodal analgesia; Immunization; Other, yet to be found measures
Identifying high risk patients
The selective tendency to develop CNCP is still poorly understood
The concept of “high risk pain patient” should be recognized similar to high risk cardiac or pulmonary patients
Probably depends on genetic and phenotypic characteristics
Genetic markers for CNCP
The tendency to develop chronic pain in rats is 30-70% genetic1
Strong indications in humans: Haplotypes of the gene encoding catecholamine-O-methyltransferase (COMT) could distinguish between patients that will have low, moderate or high experimental pain levels2
1Mogil JS, et al., Pain 80;67:1999; 2Diatchenko L, et al., Hum Mol Genet 14;135:2005
Phenotypic markers
Previous exposure to painful stimuli Early life adversities Basic sensitivity to painful stimuli1
1Granot M, et al., Anesthesiology 98;1422:2003
The environment
Social conditions: Living in a socially compromised housing area
was significantly associated with increased chronic musculoskeletal pain1
1Bergman-S, et al., J Rheumatol 28;1368:2001
The food we eat
Supplementing rats with soy protein-rich diet before, but not after surgical nerve injury prevents the development of chronic neuropathic pain-like syndrome1
1Shir Y, et al., Anesthesiology 95;1238:2001
Practical approach to prevent some types of CNCP?
Be familiar with possible predictors (personal & family history, cultural, ethnical & social background, psychological risk factors)
Categorize level of risk Consider suitable preemptive (preventive) therapy Listen to your patients
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Immunization against (neuropathic) pain?
A study done in the USA1: In almost 40,000 older adults Early herpes zoster vaccination resulted in:
Reduced incidence of acute shingles (51%) Reduced incidence of chronic shingles pain
(66%)
1Oxman MN et al. N Engl J Med 352;2271-84:2005
Post herpetic neuralgia
• 1 million new cases/year in the USA• 15% will develop PHN• In patients > 70 years old the chances for PHN are
up to 70% (52)• Refractory to most common therapies
Controlling the brain
Following training humans can control activation of specific brain regions involved with nociception, resulting in significant pain relief1
1deCharms RC, et al, Proc Natl Acad Sci U S A 102;18626-31:2005
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When to refer patients with CNCP to a pain specialist?
Uncontrolled pain Significant disability A comorbid psychiatric disorder Diagnostic evaluation for unknown etiology Consultation for treatment recommendations Need for treatment modalities that the PCP cannot
provide
Thank you
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