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

• (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

• (A) Glutamate

Answer

Which of the following physiologic pain types would best be treated with anti inflammatory agents?

(A) Neuropathic (B) Nociceptive (C) Muscular (D) Chronic

• (B) Nociceptive

Answer

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

• (B) False

Answer

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

• (A) Knee

Answer

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

• A) True

Answer

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 anti inflammatory 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

• Nausea • Disability • Light sensitivity • C) 1,2,3

Answer

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

• 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

• B) False

Answer

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)

•

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

• 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

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

• 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

• •

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

psoriatic arthritis, inflammatory bowel-related arthritis 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

• •

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

distress pain, maintain function, and manage psychosocial •

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 back mobilizing 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

• •

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

• 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

• hormones (

eg, menstrual migraine)

• sleep (too much or too little) • Stress • physical exertion • environment (

eg, bright lights, allergens)

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

medication of preventive

Comorbidities

• 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

• • • • • • • • • • • • • • • • •

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

• 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

• 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) 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

— 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

• 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 [ 34 36 ]. 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

• 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. Only propranolol and timolol have been approved by the US Food and Drug Administration (FDA) for this indication, but metoprolol , nadolol , and atenolol 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 that topiramate 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 include pregabalin (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

• • • • • • • • • • • •

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

• • • • • • • • • 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

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

•

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

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

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

•

opioid agreement

• urine drug screen • discuss expectations • Set goals; discuss and determine signs of success

Monitoring

•

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