Chronic Pain 2010

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Chronic Pain 2010

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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. - PowerPoint PPT Presentation

Transcript of Chronic Pain 2010

Page 1: Chronic Pain 2010

Chronic Pain 2010

Page 2: 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

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Answer•

(B) Is independent of the original cause of pain

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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

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Answer

• (A) Glutamate

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Which of the following physiologic pain types would

best be treated with anti-inflammatory agents?

(A) Neuropathic (B) Nociceptive

(C) Muscular (D) Chronic

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Answer

• (B) Nociceptive

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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

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Answer

• (C) Treating acute pain same as chronic pain

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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

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Answer

• (B) Feeling obligated to control patient’s pain

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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

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Answer

• (D) Believing chronic pain can be eliminated completely

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Opioids are the gold standard for treatment of

chronic pain.(A) True (B) False

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Answer

• (B) False

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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

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Answer

• (A) Pain intensity returns to baseline

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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

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Answer

• (D) All the above

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The Diagnosis, Intractability, Risk, and Efficacy (DIRE) score assesses

which of the following whenconsidering 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

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Answer

• (D) All the above

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All the following are features of fibromyalgia, except:

(A) Unilateral musculoskeletal pain

(B) Musculoskeletal pain lasting ≥3 mo

(C) Fatigue (D) Mood disturbances

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Answer

• (A) Unilateral musculoskeletal pain

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Pain at which of the following sites is included in the criteria for fibromyalgia by The American

College ofRheumatology?

(A) Knee (B) Scalp (C) Back of forearm (D) Thumb

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Answer

• (A) Knee

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In patients with fibromyalgia, decreased secretion of _______ can lead to sleep disturbances.

(A) Substance P (B) Cortisol

(C) Growth hormone (D) Dopamine

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Answer

• (B) Cortisol

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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

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Answer

• (B) Low-impact cardiovascular exercise

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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

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Answer

• Duloxetine and pregabalin

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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

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Which of the following are indicative of a back disorder with nerve root involvement?

1. Leg pain that is worse than back pain2.Weakness of ankle and great toe

dorsiflexion3. 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

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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

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 Patients with spinal stenosis frequently find relief upon sitting

or bending forward. A) True B) False

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Answer

•  A) True

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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

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Answer

• A) Nonspecific low back pain

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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

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Answer

•  A) Acetaminophen

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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

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Answer

•  B) Superficial heat

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Which of the following symptoms is(are) characteristic of migraine?

1. Nausea2. Disability

3. Light sensitivity4. Dry mouth

 A) 1 B) 1,2

 C) 1,2,3 D) 1,2,3,4

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Answer

• Nausea

• Disability

• Light sensitivity

•  C) 1,2,3

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Common triggers of migraine include which of the following?

 A) Environmental allergens B) Excess sleep C) Hormones

 D) All the above

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Answer

•  D) All the above

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Signs and symptoms of underlying organic disease in the patient with headache include

which of the following?1. Systemic symptoms

2. Neurologic symptoms3. Sudden onset

4. Onset in patient >50 yr of age5. Deviation from previous headache history

 A) 1,3,5 B) 2,3,4 C) 1,2,4

 D) 1,2,3,4,5

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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

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Chronic tension-type headache is associated

with nausea and vomiting. A) True B) False

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Answer

• B) False

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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 

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Answer

• B) Common in older patients

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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;

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Answer

• A. Hemicrania continua

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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

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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

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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 

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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

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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

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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 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

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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

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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

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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 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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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?

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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)

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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

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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

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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)

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Migraine triggers• 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

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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

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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)

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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

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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)

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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

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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

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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

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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

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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.

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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. 

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• 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

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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.

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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.

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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.

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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.

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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.

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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. 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.

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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.

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 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.

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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

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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

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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. 

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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

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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

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Pain assessment

• determine time course of pain (ie, whether pain acute, chronic, or recurrent)

• Recognize and treat physiologic pain types

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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

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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

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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”])

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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?”)

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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

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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

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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)

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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)

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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

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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

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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

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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

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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

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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

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Initiating prescription management

• opioid agreement

• urine drug screen

• discuss expectations

• Set goals; discuss and determine signs of success

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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