Transcript 1 - Dr. T. Howard Black

Chronic Pain 2010
Chronic pain:
(A) Has a predictable end
(B) Is independent of the original
cause of pain
(C) Is curable with opioids
(D) Rarely becomes a
biopsychosocial problem
Answer
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(B) Is independent of the original cause of
pain
Which of the following
neurotransmitters is associated
with the mediation of acute,
normal, or adaptive pain?
(A) Glutamate
(B) Substance P
(C) Cholecystokinin
(D) Brain-derived neurotrophic
factor
Answer
• (A) Glutamate
Which of the following
physiologic pain types would
best be treated with antiinflammatory agents?
(A) Neuropathic
(B) Nociceptive
(C) Muscular
(D) Chronic
Answer
• (B) Nociceptive
Lumping
• (A) Engaging in high-risk treatments with
• noncompliant patients
• (B) Feeling obligated to control patient’s
pain
• (C) Treating acute pain same as chronic
pain
• (D) Believing chronic pain can be
eliminated completely
Answer
• (C) Treating acute pain same as chronic
pain
Servitude
• (A) Engaging in high-risk treatments with
• noncompliant patients
• (B) Feeling obligated to control patient’s
pain
• (C) Treating acute pain same as chronic
pain
• (D) Believing chronic pain can be
eliminated completely
Answer
• (B) Feeling obligated to control patient’s
pain
Perfectionism
• (A) Engaging in high-risk treatments with
• noncompliant patients
• (B) Feeling obligated to control patient’s
pain
• (C) Treating acute pain same as chronic
pain
• (D) Believing chronic pain can be
eliminated completely
Answer
• (D) Believing chronic pain can be
eliminated completely
Opioids are the gold
standard for treatment of
chronic pain.
(A) True (B) False
Answer
• (B) False
Choose the correct statement about
flares of chronic pain.
(A) Pain intensity returns to baseline
(B) Medication doses should be
increased with every episode
(C) Flares are a sign of worsening
disease
(D) Changes in pain quality and
physical findings are common with
flares
Answer
• (A) Pain intensity returns to baseline
Which of the following is a form
of noncompliance?
(A) Increasing medication doses
without authorization
(B) Nonparticipation in
recommended therapies
(C) Illegal drug use
(D) All the above
Answer
• (D) All the above
The Diagnosis, Intractability, Risk,
and Efficacy (DIRE) score assesses
which of the following when
considering patients for opioid use?
(A) Psychologic health
(B) Social support
(C) Level of motivation to
participate in an array of treatments
(D) All the above
Answer
• (D) All the above
All the following are features of
fibromyalgia, except:
(A) Unilateral musculoskeletal
pain
(B) Musculoskeletal pain lasting
≥3 mo
(C) Fatigue
(D) Mood disturbances
Answer
• (A) Unilateral musculoskeletal pain
Pain at which of the following
sites is included in the criteria for
fibromyalgia by The American
College of
Rheumatology?
(A) Knee (B) Scalp (C) Back of
forearm (D) Thumb
Answer
• (A) Knee
In patients with fibromyalgia,
decreased secretion of _______
can lead to sleep disturbances.
(A) Substance P
(B) Cortisol
(C) Growth hormone
(D) Dopamine
Answer
• (B) Cortisol
Which of the following
nonpharmacologic therapies
appears to have greatest efficacy
in patients with fibromyalgia?
(A) Strength training
(B) Low-impact cardiovascular
exercise
(C) Chiropractic therapy
D) Acupuncture
Answer
• (B) Low-impact cardiovascular exercise
Which of the following are
approved by the Food and Drug
Administration (FDA) for the
treatment of fibromyalgia?
(A) Amitriptyline and
duloxetinev
(B) Duloxetine and pregabalin
(C) Pregabalin and fluoxetine
(D) Fluoxetine and citalopram
Answer
• Duloxetine and pregabalin
Choose the correct statement
about tramadol.
(A) 200 times more potent than
morphine
(B) Side effects include increased
risk for seizures
(C) Onset of action slow
(D) Duration of action long
Which of the following are indicative of a
back disorder with nerve root involvement?
1. Leg pain that is worse than back pain
2.Weakness of ankle and great toe
dorsiflexion
3. No relief with bed rest
4. Unilateral neurologic symptoms in foot
A) 1,3
B) 1,2,3
C) 1,2,4
D) 1,2,3,4
Answer
• Leg pain that is worse than back pain
• Weakness of ankle and great toe
dorsiflexion
• Unilateral neurologic symptoms in foot
• C. 1,2,4
Patients with spinal stenosis
frequently find relief upon sitting
or bending forward.
A) True
B) False
Answer
• A) True
Which of the following is not a
justification for ordering
radiographic testing?
A) Nonspecific low back pain
B) Progressive neurologic
deficits
C) Signs of radiculopathy
D) Suspected spinal stenosis
Answer
• A) Nonspecific low back pain
All the following medications
were shown to be superior to
placebo for pain relief in acute
low back pain, except:
A) Acetaminophen
B) Nonsteroidal antiinflammatory drugs (NSAIDs)
C) Skeletal muscle relaxants
D) All the above
Answer
• A) Acetaminophen
Which of the following
nonpharmacologic therapies was
shown to be effective in the
treatment of acute low back pain?
A) Bed rest
B) Superficial heat
C) "Back school" program
D) None of the above
Answer
• B) Superficial heat
Which of the following symptoms is(are)
characteristic of migraine?
1. Nausea
2. Disability
3. Light sensitivity
4. Dry mouth
A) 1
B) 1,2
C) 1,2,3
D) 1,2,3,4
Answer
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Nausea
Disability
Light sensitivity
C) 1,2,3
Common triggers of migraine
include which of the following?
A) Environmental allergens
B) Excess sleep
C) Hormones
D) All the above
Answer
• D) All the above
Signs and symptoms of underlying organic
disease in the patient with headache include
which of the following?
1. Systemic symptoms
2. Neurologic symptoms
3. Sudden onset
4. Onset in patient >50 yr of age
5. Deviation from previous headache history
A) 1,3,5
B) 2,3,4
C) 1,2,4
D) 1,2,3,4,5
Answer
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Systemic symptoms
Neurologic symptoms
Sudden onset
Onset in patient >50 yr of age
Deviation from previous headache history
D) 1,2,3,4,5
Chronic tension-type
headache is associated
with nausea and
vomiting.
A) True
B) False
Answer
• B) False
Which of the following is not a
characteristic of new daily
persistent headache?
A) Highly refractory to treatment
B) Common in older patients
C) Often associated with viral
illness
D) Begins abruptly and fails to
remit
Answer
• B) Common in older patients
What Headache is rare, an
indomethacin-responsive headache
Continuous and unilateral, with migraine
and autonomic features
(eg, tearing, ptosis, mydriasis)
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A. Hemicrania continua
B. hemiplegic migraine
C. basilar migraine
D. migraine with prolonged aura (>60 min;
Answer
• A. Hemicrania continua
Back Pain
• Evaluation: American College of Physicians
and American Pain Society issued new clinical
guidelines in 2007
• Urge use of patient history and physical
examination to categorize back pain as associated
with 1 of 3 etiologies
• 1) nonspecific (most common etiology; usually of
mechanical origin)
• 2) associated with neurologic symptoms (radicular
pathology or stenosis of spinal canal)
• 3) systemic causes
• psychosocial issues also important
Physical examination
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Indicators of nerve root involvement
leg pain worse than back pain
positive straight-leg-raise test
unilateral neurologic symptoms in foot
weakness of ankle and great toe
dorsiflexion
• loss of ankle reflexes
Neurologic testing
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For patients suspected of having a disc herniation, neurologic testing should
focus on the L5 and S1 nerve roots, since 98 percent of clinically important
disc herniations occur at L4-5 and L5-S1
L5 motor nerve root testing evaluates strength of ankle and great toe
dorsiflexion. L5 sensory nerve root damage would result in numbness in the
medial foot and the web space between the first and second toe.
The S1 nerve root is tested by evaluating ankle reflexes and sensation at the
posterior calf and lateral foot. S1 radiculopathy may cause weakness of plantar
flexion, but is difficult to detect until quite advanced. One strategy is to have
the patient raise up on tip-toe three times in a row, on one foot alone and then
the other.
Although ankle reflexes are an important part of S1 nerve root testing, the
absence of ankle reflexes becomes increasingly common with age. Among
patients without a known pathologic cause of abnormal reflexes, most patients
under age 30 have intact ankle reflexes [44]. However, absent reflexes were
found in 30 percent of those between ages 61 and 70 and nearly 50 percent of
those ages 81 to 90. Unilateral absence of ankle reflexes was found to be
uncommon, though, occurring in only 10 percent of those over age 60.
Therefore, unilateral absence of an ankle reflex is rare enough to be a
clinically useful sign, with a specificity of 89 percent
Straight-leg-raise test
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variability in literature on how to perform
patient lies supine
physician flexes hip with leg extended
Lasegue sign positive if flexion (usually at
30) provokes leg pain
next, lower leg slightly, and have patient
dorsiflex ankle
• resulting pain positive Bragard sign
• can also test hip flexion with knee flexed
Features suggestive of
spinal stenosis
• severe leg pain that limits distance patient able to
walk
• relief upon sitting or bending forward
• patients may describe pain as burning (suggests
vascular pain, thus term pseudoclaudication)
• patients may have both pseudoclaudication and
claudication
• wide-based gait with abnormal neurologic
findings (positive Romberg test) and pain with
lumbar extension
• uncommon in patients <50 yr of age
Systemic causes
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1% to 2% of low back pain
Compression fracture—advanced age with steroid therapy
Trauma
cancer (nondermatologic)—unexplained weight loss
No relief with bed rest
increased age
symptoms >1 mo
spondyloarthropathies—eg, ankylosing spondylitis, reactive arthritis,
psoriatic arthritis, inflammatory bowel-related arthritis
morning stiffness
improvement with exercise
extra-articular symptoms
infection—recurrent or chronic urinary tract infections
history of intravenous drug use
fever
Psychosocial factors
• patients with severe psychosocial and
emotional problems, (eg, depression) more
likely to develop back pain and have worse
prognosis
• study showed correlation between heavy
workload, stress, and back pain
• treatment of psychosocial factors more
important than physical factors
• patients who take ownership of their pain
and actively participate in care have better
outcomes
Radiographic evaluation
• recent guidelines advise against routine imaging and other diagnostic
tests in patients with nonspecific low back pain
• reserve imaging for patients with severe or progressive neurologic
deficits, or patients with suspected serious underlying conditions (eg,
radiculopathy, systemic illness)
• when pain persistent and signs of radiculopathy or spinal stenosis
present, think beyond imaging
• (eg, in patients unwilling to undergo surgery, advise that MRI not
recommended)
• no consensus on when to follow negative x-rays with more advanced
tests, or when to proceed immediately with advanced tests (eg, MRI,
computed tomography [CT])
• study showed higher satisfaction reported among patients with low
back pain when x-rays done, despite more severe pain and lower
function scores
• must balance costs and patient satisfaction
Classification by duration and goals
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acute—<4 wk
Most common type
intervention usually unnecessary
Reassure patient that spontaneous recovery likely
subacute—4 to 12 wk
dynamic group
some patients improve, others slip into chronic group
consider whether intervention suitable
chronic—>12 wk
discuss management with patient
stress that patient must be leader in care
goals—control pain, maintain function, and manage psychosocial
distress
• recommendations—provide patients with prognostic information based
on duration of symptoms and clinical presentation
• advise patients to remain active
• direct them to appropriate educational resources
Drug therapies
• Acetaminophen: acute back pain—no
difference seen between acetaminophen and
no treatment
• chronic back pain—acetaminophen slightly
inferior to nonsteroid anti-inflammatory
drugs (NSAIDs)
• insufficient data comparing acetaminophen
to other drugs
NSAIDs
• acute back pain—nonselective NSAIDs
(cyclooxygenase [COX]-1 and COX-2
inhibitors) superior to placebo for global
improvement
• chronic back pain— NSAIDs better than
placebo
• ineffective in back pain with sciatica
• no evidence one NSAID superior to another
• patients frequently have clear preferences
Antidepressants
• better than placebo for pain relief in chronic
back pain
• effectiveness not consistent across classes
• tricyclic antidepressants (TCAs) slightly to
moderately more effective than placebo
• paroxetine and trazodone ineffective
• insufficient evidence comparing TCAs to
selective serotonin reuptake inhibitors
Other Medications
• Benzodiazepines acute back pain—studies
showed high likelihood of failure to
experience pain relief or global
improvement with tetrazepam
• Antiepileptic agents: back pain with
radiculopathy—minor improvements in
pain scores
• no clear changes in functional status
• Skeletal muscle relaxants acute back pain—
moderately superior to placebo for pain
relief
• sciatica—no effectiveness observed
Other Medications
• Tramadol: chronic back pain—moderately superior to
placebo for pain relief
• no trials comparing tramadol to acetaminophen, NSAIDs,
or opioids
• Systemic corticosteroids (oral, intravenous, and
intramuscular): no systematic reviews
• 4 trials showed no clinically significant benefit, compared
with placebo
• Opioids: review looked at prevalence of use and abuse, and
effectiveness
• prescribing rates varied widely (3%-66%);
• 4 trials showed pain similar with opioids and either active
treatment or placebo
• rate of substance abuse disorders varied from 5% to 24%;
overall study quality weak
Nonpharmacologic
therapies
• acute back pain—of numerous modalities
studied, only superficial heat demonstrated
efficacy
• chronic or subacute back pain—benefit seen
with spinal manipulation, exercise therapy,
psychologic therapy and interdisciplinary
rehabilitation
Bed rest vs activity
• activity distinguished from exercise;
defined as activity of normal daily living
• 1995 Helsinki study showed activity
superior to either bed rest or backmobilizing exercise
• systematic reviews found more pain and
impairment of function with bed rest than
with activity
Injection therapy
• subacute and chronic back pain—
• Cochrane review unable to find evidence
for or against injection therapy, regardless
of type or dosage
• may be effective for subgroup of patients
A Practical Approach to
Patients with Headache
• Diagnosis
• History: detailed history usually provides
enough information for diagnosis
• physical examination normal in most cases
• rule out alternative etiologies
• address impact of headache on patient
• look for red flags
• classify headache most headaches migraine
A Practical Approach to
Patients with Headache
• useful questions—when did worst headaches
begin?
• frequency of headaches that if untreated impair
ability to function?
• description and duration of pain
• do other symptoms accompany headaches?
• what improves or worsens headaches?
• frequency and type of medication taken for
headaches?
• others in family with similar headaches?
• does patient get other kinds of headaches?
• any recent change in headaches?
Clinical features
• nature of pain (eg, dull, throbbing, shooting,
burning)
• severity; duration; frequency
• Exacerbation with physical exertion
• nausea; vomiting
• sensitivity to light, sound, odors
• neck pain and muscle tension
• Physical changes (eg, tearing eyes,
sweating)
Criteria for migraine
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presence of 3 characteristics
nausea
Disability
light sensitivity
confirms migraine
if 2 of 3 positive, 93% chance headache
migraine; if 3 of 3 positive, 98% chance
headache migraine
Migraine without aura
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duration 4 to 72 hr
frequency <15 days/mo
pain features (2 required)—
unilateral location
pulsating quality
moderate to severe pain intensity
aggravation by or causing avoidance of routine
physical activity
• nonpain features (1 required)—nausea or
vomiting
• photophobia and phonophobia
• must not be attributable to another disorder
Migraine with aura
• 30% to 35% of migraines
• aura defined as transient, slowly emerging (then
regressing) neurologic symptoms
• usually precede headache by hr
• Visual aura—most common
• scintillating scotoma (dark spot with shimmering rim)
• fortification spectra (jagged lines)
• photopsia (colored splotches, flashes of light)
• Sensory aura—tingling, numbness, paresthesias
• spreads slowly
• often beginning in hand or mouth
• other auras—less common (eg, weakness, aphasia)
Migraine triggers
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hormones (eg, menstrual migraine)
sleep (too much or too little)
Stress
physical exertion
environment (eg, bright lights, allergens)
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Past treatment
inquire about past use of acute medications
pain medications
NSAIDs, opioids, and migraine-specific drugs
preventive medications
antidepressants,
Anticonvulsants
Antihypertensives
supplements
reasons for discontinuation
Ineffectiveness
side effects;
inadequate length of trial
unsuitable medication
note—overuse of acute medication may impede efficacy of preventive
medication
Comorbidities
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Depression
Anxiety
Epilepsy
fibromyalgia
Hypertension
Diabetes
vascular disease
Benign indicators
regular or near-regular perimenstrual
Timing
appearance after sustained exertion
relief with sleep; food, odor, or weather triggers
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Signs and symptoms of
organic disease
abnormal signs
(fever, hypertension, or hypotension)
altered cognition or consciousness
stiff neck (meningeal irritation)
Papilledema (increased intracranial pressure)
unequal or poorly reactive pupils
visual field deficit
tender, poorly pulsatilecranial arteries (especially in patients aged >50 yr)
Focal weakness or sensory loss
clumsiness or ataxia
red flag mnemonic (“SSNOOP”)
Systemic symptoms
Secondary risk factors
Neurologic symptoms abnormal signs
Onset (sudden, abrupt, or split-second)
Older (new onset at age >50 yr;)
Previous headache history (first headache or change in headache)
Migraine treatments
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Acute therapy
nonspecific medications—NSAIDs
combination analgesics
Opioids
neuroleptics and antiemetics
corticosteroids (for refractory migraine)
Specific medications—ergotamine and
dihydroergotamine
• triptans
• general principles—tailor treatment to patient and
attack
• treat early
Migraine treatments
• nonpharmacologic treatment, when appropriate (eg, rest, quiet, hot or
cold compress, massage, meditative exercise)
• use acute medications in stratified manner (first-line, backup, and
rescue)
• Match intensity of treatment to intensity of attack
• mild to moderate pain—usually responsive to nonspecific treatment
• moderate to severe pain—migraine-specific treatments
• can be mixed with nonspecific treatments
• If unsuccessful, resort to neuroleptics, opioids, or shortcourse
corticosteroids
• Food and Drug Administration (FDA)-approved acute treatments
• aspirin, ibuprofen, ergots, triptans, combination acetaminophen,
aspirin, and caffeine (eg, Excedrin Migraine)
Medication overuse
• limit use of ergots, triptans, opioids or
simple combination analgesics to 10
days/mo
• Butalbitalcontaining analgesics 5 days/mo
• other analgesics 15 days/mo
• total exposure (all acute drugs combined)
15 days/mo
• consequences of overuse—refractory daily
Headaches
• tolerance to medications
• drug toxicity
Preventive treatment
• indications—migraine significantly interfering with patient’s daily
routine, despite acute treatment
• >1 attack per week
• acute medications ineffective, contraindicated, or not tolerated
• patient preference
• presence of uncommon migraine symptoms, eg, hemiplegic migraine,
basilar migraine, migraine with prolonged aura (>60 min; can lead to
migrainous infarction)
• medications—anticonvulsants
• antidepressants
• (most commonly TCAs and serotonin-norepinephrine reuptake
inhibitors)
• blood pressure medications (including angiotensin system drugs)
• supplements (eg, riboflavin, coenzyme Q10)
• botulinum neurotoxin (for chronic migraine)
• drug choice depends on headache type, drug efficacy and adverse
events, current drug regimen, patient preference, and comorbidities
Protocol
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start with low dose and increase gradually
Ensure adequate drug trial (2-3 mo)
avoid drug overuse and interfering drugs
evaluate efficacy of therapy
(patients use calendar to record headache
frequency and treatment usage)
• Periodically re-evaluate suitability of
treatment
• ascertain use of birth control
Chronic daily headaches (CDH)
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treatment often fails
Patients frequently overusing medication and have comorbid psychologic disturbances
4% of world population has CDH
previously referred to as mixed or combination headache
criteria—evolves from episodic to chronic pattern
frequency increases
intensity may weaken while migrainous features abate
daily or near-daily (15 days/mo)pain
chronic tension-type headache—mild to Moderate
15 days/mo for 3 mo
not associated with nausea or vomiting
tension-like characteristics (dull, featureless)
new daily persistent headache—begins abruptly and fails to remit
often associated with viral illness
Frequently no identifiable trigger or cause
can be highly refractory to treatment
common in younger patients
features similar to chronic migraine
Hemicrania continua—rare, indomethacin-responsive headache
Continuous and unilateral, with migraine and autonomic features
(eg, tearing, ptosis, mydriasis)
typically moderate baseline pain with severe exacerbations
First-line agents Chronic Migraine
• — In clinical practice, the same prophylactic medications used for
episodic migraine are used for the prevention of chronic migraine.
Thus, first-line prophylactic medications for chronic migraine include:
• Beta blockers (propranolol, metoprolol, timolol)
• Amitriptyline
• Topiramate
• Valproic acid and its derivatives
• We suggest that treatment for patients with chronic migraine begin
with trials of one of these agents. (See "Preventive treatment of
migraine in adults".)
• It is expected that up to 50 percent of patients treated with one of these
medications will have at least a 50 percent reduction in the frequency
of headaches after three months of treatment, given adequate doses.
However, side effects are common and may limit the use of these
prophylactic agents.
Second-line agents for
Chronic Migraine
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— For patients with chronic migraine that is refractory to adequate trials of first-line agents, a
number of other drugs are potential alternatives, including the following:
Botulinum toxin injections [29-31]
Butterbur
Calcium channel blockers
Feverfew
Fluoxetine
Gabapentin
Levetiracetam
Magnesium
Memantine
Pregabalin
Riboflavin
Serotonin-norepinephrine reuptake inhibitors
Tizanidine [32]
Of note, botulinum toxin injection is not recommended for the treatment of episodic migraine, but
randomized trials evaluating botulinum toxin injection for chronic migraine have yielded mixed
results [29-31]. The effectiveness of the remaining second-line medications for episodic and chronic
migraine is also uncertain, as most have been studied only on a limited basis.
• Regardless of the drug chosen, application of
certain principles may improve the success rate of
prophylactic migraine therapy and reduce
complications:
• Start oral drugs at a low dose and increase
gradually
• Give the chosen medication an adequate trial
• Avoid overuse of acute headache medications
• Avoid valproate for women of childbearing
potential
• Address patient expectations and preferences
Riboflavin
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A randomized, double-blind, placebo-controlled study of
55 patients who were suffering from two to eight
migraines per month found that the administration of
oral riboflavin at a dose of 400 mg/day compared with
placebo resulted in a significantly higher proportion of
patients with greater than 50 percent improvement in the
frequency of headaches (54 versus 19 percent), headache
days (57 versus 15 percent), and the migraine index
(headache days and mean severity, 39 versus 8 percent)
[56]. The benefits only became significant after three
months of therapy. Riboflavin was well tolerated.
Additional studies are needed to confirm these results and
to determine the optimum dose and patient population
most likely to benefit.
Feverfew
• Feverfew has been the herbal remedy most studied for the
prevention of migraine, but evidence regarding benefit is
conflicting. A systematic review of feverfew for migraine
prophylaxis found five randomized controlled trials with
343 patients that met the inclusion criteria [39]. While
three of the trials [40-42] found that feverfew was
effective, the two trials with the highest methodologic
quality [43,44] found no significant difference between
feverfew and placebo [39]. The review concluded that trial
results were mixed and did not establish that feverfew is
more effective than placebo for the prevention of migraine.
The safety of this and other herbal products is unknown.
Coenzyme Q10
• Interest in coenzyme Q10 (CoQ10)
and riboflavin (see'Riboflavin' below) for migraine
treatment has been sparked by the potential role of
mitochondrial dysfunction in migraine pathogenesis [37].
• In a small, randomized controlled trial of 42 patients with
migraine, Coenzyme Q10 (CoQ10) was effective for
migraine prophylaxis; significantly more patients treated
with CoQ10 (100 mg three times daily) experienced a ≥50
percent reduction in attack frequency (the primary outcome
measure) at three months than patients treated with placebo
(47.6 versus 14.4 percent) [38]. CoQ10 treatment was well
tolerated. Larger clinical trials are needed to confirm the
benefit of CoQ10 for migraine prevention.
Butterbur
• An extract of Butterbur (Petasites hybridus) root, a perennial shrub, is
an herbal medicine that is marketed as a food supplement in the United
States and as a licensed pharmaceutical medicine in Germany
(Petadolex). At least two small placebo-controlled clinical trials have
found some efficacy for Petasites extract in migraine prevention [3436]. In the larger of these studies, Petasites at a dose of 75 mg but not
50 mg daily was effective and well tolerated as preventive therapy for
migraine. Gastrointestinal upset, predominately burping, was the most
common side effect [36].
• Butterbur contains pyrrolizidine alkaloids, potential carcinogens that
are removed from the commercially prepared Petasites root extract. No
part of the Petasites plant should be ingested other than the commercial
products.
ANTICONVULSANTS
• The anticonvulsants sodium
valproate,gabapentin, and topiramate are
more effective than placebo for reducing the
frequency of migraine attacks [19]. Both
valproate and topiramate are approved by
the US FDA for migraine prophylaxis.
Beta blockers
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Several randomized, placebo-controlled studies have found that
chronic therapy with propranolol reduces the frequency and severity of
migraine in 60 to 80 percent of patients [6,7]. A subsequent systematic
review found clear evidence that propranolol is more effective than
placebo in the short-term treatment of migraine [8]. However, many of
the included trials had methodological shortcomings, and evidence
from clinical trials on long-term effects is lacking.
• Other beta blockers may also be used for migraine prophylaxis.
Onlypropranolol and timolol have been approved by the US Food and
Drug Administration (FDA) for this indication,
but metoprolol, nadolol, andatenolol are commonly used [9]. It can
take several weeks for these drugs to become effective [7]; the dose
should be titrated and maintained for at least three months before
deeming the medication a failure.
Topiramate
• Several placebo-controlled studies have found
thattopiramate is effective prophylactic therapy for
migraine [24-27]. The starting topiramate dose in most of
these studies was 25 mg/day in these studies, with slow
titration by 25 to 50 mg/week to the maximum of 100 mg
twice daily or the highest tolerated dose. Topiramate is
approved for migraine prophylaxis by the US FDA.
• Topiramate treatment-related adverse events, generally
mild to moderate in severity, included paresthesia, fatigue,
anorexia, diarrhea, weight loss, hypesthesia, memory
difficulty, language problems, difficulty with
concentration, nausea, and taste perversion. Of these,
paresthesia was the most common, occurring in about half
of patients receiving topiramate at 100 or 200 mg/day.
Weight loss is a unique side effect of this drug, and it
occurred in 9 to 12 percent of patients taking 100 to 200
mg/day of topiramate.
Complex regional pain
syndrome
• (CRPS) is a disorder of the extremities that
is characterized by pain, swelling, limited
range of motion, vasomotor instability, skin
changes, and patchy bone demineralization.
• It frequently begins following an injury,
surgery, or vascular event such as a
myocardial infarction or stroke.
Pharmacologic approaches
• Only a few pharmacologic agents have
been studied in well designed clinical trials
in patients with CRPS. Medications that
appear to be significantly better than
placebo in relieving pain due to CRPS
include some agents in the following drug
classes [15]:
• Anticonvulsants
• Bisphosphonates
• Oral glucocorticoids
• Nasal calcitonin
Complex regional pain syndrome
• Though not specifically studied in CRPS,
antidepressant medications are often effective in
reducing neuropathic pain. The author's clinical
experience suggests that tricyclic antidepressants
reduce pain and are a valuable addition to physical
therapy for patients with CRPS.
• Guidelines developed by a consensus of experts in
CRPS suggest beginning treatment for pain due to
CRPS with a tricyclic antidepressant
(eg, amitriptyline or nortriptyline), an
anticonvulsant (eg, gabapentin), a nonsteroidal
antiinflammatory drug, and, for those with severe
pain, with an opioid
Anticonvulsants
• Anticonvulsants are beneficial in chronic
pain, particularly with pain that is
lancinating, burning, or sharp. Successful
use in some cases of CRPS Type I has been
reported for gabapentin [16,17]. Newer
agents includepregabalin (75 mg twice
daily) or lamotrigine (25 mg twice daily).
Although unproven in CRPS, these drugs
have a good margin of safety and may be
useful if NSAIDs and amitriptyline are
inadequate for pain management.
Definitions and characteristics
• acute pain—has beginning, middle, and
predictable end point
• Chronic pain—persists beyond expected
time
• independent of original cause
• not curable
• often becomes biopsychosocial problem
Pathophysiology of pain
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glutamate—neurotransmitter
contained in glutamate vesicles; mediates acute, normal, or adaptive pain
other neurotransmitters—eg, substance P, cholecystokinin, brain-derived neurotrophic
factor, calcitonin gene-related peptide\
contained in dense-core vesicles mediate chronic, inflammatory, persistent, neuropathic,
pathologic
ongoing pain families of nerve pairs carry predominantly glutamate or predominantly
nonglutamate neurotransmitters
morphine less effective at blocking pathologic pain mediated by neurokinin and
Nmethyl-D-aspartate receptors spontaneous ectopic firing—in dorsal horn of spinal
cord, first synapse from unmyelinated pain nerve can result in spontaneous firing of
nerve anywhere along nerve pathway
Ephaptic impulse generation—injured nerve trunk that includes non–pain-associated
nerves (eg, A- fibers that carry touch, pressure, vibration) can result in
“short circuiting” to pain nerve
even light touch can result in shock of pain
deafferentation pain—on other side of synapse, sufficient damage to peripheral system
can result in automatic firing of secondorder neuron without input
central sensitization— upregulation of second-order neurons with persistent pain
glial cells can generate and trigger pain signaling
Pain assessment
• determine time course of pain (ie, whether
pain acute, chronic, or recurrent)
• Recognize and treat physiologic pain types
Treatment of physiologic pain types
• psychogenic—treat anxiety or depression
• nociceptive—inflammatory or mechanical pain
• treat with anti-inflammatory agent, or stabilize or decompress
mechanical cause of pain
• neuropathic—treat with drugs (eg, anticonvulsants, antidepressants)
• muscular—manage with physical rehabilitation approach
• consider muscle relaxant or botulinum toxin type A (eg, Botox)
• acute pain—treat with opioids, regional blocks for localized acute pain,
and medical and surgical interventions treat underlying disease
• chronic pain—manage with self-care strategies, behavioral methods,
long-term medications, complementary therapies, and
multidisciplinary care
• widespread pain—eg, fibromyalgia; treat with medications that affect
entire body; manage with general exercise rehabilitation approach,
mental measures (eg, relaxation techniques), education, and
psychosocial measures
• regional pain—use localized treatment (eg, topical treatment or
regional block)
• reduce pain while instituting other therapies
Contributing factors
• do not cause pain, but worsen or lengthen
duration of pain
• eg, poor posture contributes to chronic pain
after car accident
• daily gum chewing contributes to daily
headaches
• consider depression and anxiety
• treat separately
Time course of pain
• time course for acute pain to become
chronic pain varies (eg, 3-6 mo [“but that’s
arti- ficial
• some people have a time course of 1 day
and you already can see it’s chronic pain”])
Seven deadly sins” in
management of chronic pain
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1) lumping; treating acute pain same as chronic pain, or treating pain of
different mechanisms in same way
(eg, treating trigeminal neuralgia with nonsteroidal anti-inflammatory drug
[NSAID])
2) opioid worship; believing that opioids highly effective for chronic pain
opioids not gold standard for chronic pain; according to American Pain
Society guidelines, >200 mg/day of opioids “probably too high”;
3) stupidity; repeating ineffective treatment
patients who do not respond to treatment should be reassessed for contributing
factors, barriers, or different physiologic cause
4) servitude; feeling obligated to control patient’s pain
patients may threaten to obtain pain medications “on the streets”, or inflict
guilt (eg, “I just don’t think you’re giving me good pain control”)
patients must recognize pain cannot be resolved completely and that they must
work with physician (ask patient, “what are you willing to do to help your pain
improve?”)
Seven deadly sins” in
management of chronic pain
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5) perfectionism; believing chronic pain can be eliminated completely
breakthrough pain defined in cancer patients with advanced illness as 20% fluctuation in
pain intensity over 48 hr, from baseline of 72 hr
important to distinguish chronic pain from flares; assure patients that increasing dose
will not eliminate pain
advise patients that any dose of opioid can be expected to reduce pain by about 40%;
6) asking for trouble; engaging in problematic or high-risk treatments with
noncompliant or unselected high-risk patients
avoid establishing untenable treatment (eg, providing opioids to woman with bipolar
disorder and chronic back pain hospitalized for overdosing on oxycodone and
acetaminophen)
7) ignoring “elephant in office” (eg, chemical dependency, psychologic comorbidity,
patients who “need” their pain)
Personality features, anxiety, and depression contribute to and may cause pain
some patients’ lives structured around pain (ego-syntonic pain), and taking away pain
may affect structure of patient’s life
counsel patients (eg, say, “it’s obvious you’ve had your pain for a long time
we cannot eliminate your pain”)
focus on improving quality of life
opioid use
• Introduction: good outcomes of opioid
use—quality of life measurably better
• stable doses of opioids maintained over
years
• patients reliable with prescriptions
• bad outcomes of opioid use—escalating
doses
• No improvement or decline in function
• level of misery and pain score remain
constant
• patients unable to manage prescriptions
reliably
Fears associated with
prescribing opioids
• fear of loss of control of prescribing
process
• fear of regulatory scrutiny
• fear of adverse effects (eg, respiratory
depression, addiction, tolerance)
Reasons to avoid opioids
• not highly effective for chronic pain
• no studies show improvement in patient’s
function with long-term opioid use
• significant adverse effects (eg, dysphoria,
irritability, apathy, increased pain)
Flares
• temporary increase in pain intensity (ie, pain intensity returns to
baseline)
• patients perceive flare as worsening disease, or that pain medication
becoming ineffective
• medication doses often increased to treat flare, resulting in new
baseline at higher dose
• “vicious cycle” of increasing dose continues as flares occur;
pseudotolerance—apparent failure of pain medication to maintain
stable control of chronic pain, resulting in repeated dose escalations
during flares, without returning to baseline doses once flare resolves;
• distinguishing flares from progression of medical condition—increase
in pain intensity with
• unchanged distribution, quality, and physical findings most likely flare
• provide patients with tools (eg, additional 2-wk supply of medication)
to manage flares
Documentation with opioid use
• 4 As—1) analgesia;
• 2) adverse effects (eg, constipation,
sedation, drowsiness, itching, nausea) and
management
• 3) activity level, eg, changes in work hours,
ability to play with children, or walking
• 4) adherence to prescribing protocol
• initial evaluation—document pain type,
contributing
• factors, and barriers to treatment
Noncompliance
• prevalence high
• compliant patients tend to be older, and
noncompliant patients tend to be in younger
age groups (“but there is so much overlap”)
• forms—increasing dose without
authorization;
• nonparticipation in recommended therapies;
multiple
• prescribers; illegal drug use; diversion; poor
communication
• (eg, threats); alcohol abuse; declining
function due to medications
Drug screening
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of 205 patients, 78 had aberrant drug screening results
useful monitoring tool
in 27 patients, prescribed opioid not present
Cannabinoids present in 30 patients, unauthorized opioids in 11
patients,
and other unauthorized drugs (eg amphetamine) in 10 patients
presence of cocaine, alcohol, and nonprescribed amphetamine and
altered urine (eg, cold, diluted urine) found
no significant difference in addictive qualities between opioids (ie, risk
for noncompliance similar for all agents)
monitoring— important
use 1 to 2 monitoring tools
Screener and Opioid Assessment for Patients with Pain (SOAPP),
Opioid Risk Tool (ORT)
Diagnosis, Intractability, Risk, and Efficacy (DIRE) score helpful
DIRE score
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risk—1) psychologic health
2) chemical health
3) reliability
4) social support
each scored 1 to 3 (more compelling to prescribe opioids to patients with higher scores)
score of 7 to 13 predicts unsuccessful outcome
score of 14 to 21 predicts good outcome and better efficacy in pain control
diagnosis—determine how compelling diagnosis is, eg, severe peripheral vascular
disease or severe ischemic pain may be scored as 3
while muscular pain, fibromyalgia, benign conditions, or lack of diagnosis may be
scored as 1
intractability—determine patient’s level of motivation to participate in array of
treatments
consider past attempts to incorporate therapy other than drugs (eg, physical therapy,
behavioral treatments)
strong efforts may be scored as 3
patients with lack of resources, response, or interest in other therapies may be scored as
2
patients who have not tried customary treatments or have low motivation may be scored
as 1
DIRE score
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psychologic health—patients with good communication and no significant
personality dysfunction or mental illness may be scored as 3
patients with some personality issues (eg, depression, mild to moderate
anxiety) scored as 2
patients with serious personality dysfunction that impairs communication, or
patients with severe mental illness scored as 1
Chemical health—chemical copers and patients with chemical dependency in
remission may be scored as 2
Patients with no history of chemical dependence scored as 3
active users of eg, marijuana or cocaine scored as 1
reliability—patients with low social support, life in chaos, low family support,
few relationships, and loss of most life roles scored as 1
patients with supportive family, close relationships, involvement in work,
school, and other important life roles scored as 3
efficacy—patients with poor function or minimal pain relief in spite of
moderate to high opioid doses scored as 1
patients with moderate benefit with improved function, or when efficacy
unclear (eg, shortacting opioids in lower doses) scored as 2
good improvement in pain and function with stable doses over time scored as 3
Initiating prescription
management
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opioid agreement
urine drug screen
discuss expectations
Set goals; discuss and determine signs of
success
Monitoring
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monthly visits (consider more frequent
visits with higher risk patients)
occasional urine drug screening
pill count to identify noncompliance (eg,
overuse, diversion)
• consider appropriate methods of escalating
or tapering dose and withdrawing
medication
• refer patients to detoxification and/or
chemical dependency treatment as indicated