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ABPMR Pain Medicine study materials
ABPMR Pain Medicine study resources

ABPMR Pain Medicine practice questions

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Question 1Pain anatomy, physiology, and pharmacology

Which primary afferent fiber type is thinly myelinated and conveys rapid, sharp, well-localized first pain?

  1. A-delta fibers Correct answer.
  2. C fibers
  3. Preganglionic B fibers
  4. A-beta fibers

Explanation

A-delta fibers are thinly myelinated group III fibers conducting at roughly 5-30 m/s, which allows them to signal fast, sharp, punctate pain. Their terminals end mainly in lamina I and the outer part of lamina II of the dorsal horn.

Question 2Pain anatomy, physiology, and pharmacology

Which afferent population is unmyelinated, conducts slowly, and gives rise to dull, burning second pain?

  1. C fibers Correct answer.
  2. A-beta fibers
  3. A-delta fibers
  4. A-alpha motor axons

Explanation

C fibers are unmyelinated polymodal nociceptors with conduction velocities below about 2 m/s. They respond to mechanical, thermal, and chemical stimuli and terminate densely in laminae I and II, generating slow, aching, burning pain.

Question 3Pain anatomy, physiology, and pharmacology

Most opioids used clinically produce analgesia primarily by acting at which receptor?

  1. Delta opioid receptor
  2. ORL1/nociceptin receptor
  3. Kappa opioid receptor
  4. Mu opioid receptor Correct answer.

Explanation

The mu opioid receptor is a Gi/o-coupled receptor whose activation inhibits presynaptic transmitter release and hyperpolarizes postsynaptic neurons. Supraspinal, spinal, and peripheral mu receptors together produce the analgesia, respiratory depression, and constipation characteristic of clinical opioids.

Question 4Pain anatomy, physiology, and pharmacology

The analgesic action of nonselective NSAIDs depends principally on inhibition of which enzyme?

  1. Acetylcholinesterase
  2. Lipoxygenase
  3. Cyclooxygenase Correct answer.
  4. Phospholipase A2

Explanation

NSAIDs inhibit cyclooxygenase, reducing conversion of arachidonic acid to prostaglandins. Because prostaglandins sensitize peripheral nociceptors and contribute to inflammation, blocking their synthesis lowers pain and fever.

Question 5Pain anatomy, physiology, and pharmacology

Local anesthetics interrupt nerve conduction by blocking which structure?

  1. GABA-A receptors
  2. Mu opioid receptors
  3. Voltage-gated sodium channels Correct answer.
  4. Voltage-gated potassium channels

Explanation

Local anesthetics bind the inner pore of voltage-gated sodium channels, preventing sodium influx and blocking depolarization and impulse propagation. Small, unmyelinated fibers are blocked before large myelinated ones, so pain sensation is lost early.

Question 6Pain anatomy, physiology, and pharmacology

According to gate control theory, which input most directly closes the dorsal horn gate and reduces pain transmission?

  1. Blockade of inhibitory interneurons
  2. Release of substance P
  3. Activation of large-diameter A-beta fibers Correct answer.
  4. Activation of C fibers

Explanation

Gate control theory holds that large-diameter A-beta input excites inhibitory interneurons in the dorsal horn that suppress transmission from small nociceptive afferents. This is why rubbing or applying vibration can blunt pain.

Question 7Pain anatomy, physiology, and pharmacology

Which transmitter is released from the central terminals of nociceptive primary afferents and is depleted by capsaicin-sensitive neurons?

  1. GABA
  2. Substance P Correct answer.
  3. Dopamine
  4. Acetylcholine

Explanation

Substance P is released with glutamate from the central terminals of small nociceptive afferents onto dorsal horn neurons. Capsaicin-sensitive C fibers store substance P, and prolonged capsaicin exposure depletes it and defunctionalizes those terminals.

Question 8Pain anatomy, physiology, and pharmacology

Acetaminophen's analgesic effect is best explained by which mechanism?

  1. Direct mu opioid receptor agonism
  2. Central COX inhibition with reduced prostaglandin synthesis Correct answer.
  3. Irreversible COX-1 inhibition
  4. Blockade of voltage-gated sodium channels

Explanation

Acetaminophen acts largely within the central nervous system, inhibiting cyclooxygenase and lowering prostaglandin production in brain and spinal cord. This central action explains its analgesia and antipyresis with little peripheral anti-inflammatory effect.

Question 9Pain anatomy, physiology, and pharmacology

Nociceptive C fibers from the skin terminate most densely in which dorsal horn region?

  1. Lamina IX
  2. Ventral horn motor nucleus
  3. Lamina II (substantia gelatinosa) Correct answer.
  4. Dorsal column nuclei

Explanation

Fine nociceptive afferents terminate predominantly in laminae I and II, with lamina II being the substantia gelatinosa rich in modulatory interneurons. This region is a key site for opioid, adrenergic, and GABAergic control of pain input.

Question 10Pain anatomy, physiology, and pharmacology

Second-order axons of the spinothalamic tract decussate at which location?

  1. Anterior white commissure near the segment of entry Correct answer.
  2. Pyramidal decussation in the medulla
  3. Corpus callosum
  4. Internal capsule

Explanation

Spinothalamic second-order neurons cross the midline through the anterior white commissure within a few segments of entry, then ascend in the contralateral anterolateral column. This crossing pattern explains why a cord lesion produces contralateral pain and temperature loss beginning one to two segments below the level.

Question 11Pain anatomy, physiology, and pharmacology

The best-characterized descending pain-modulating pathway follows which sequence?

  1. Dorsal root ganglion to dorsal horn to thalamus
  2. Periaqueductal gray to rostral ventromedial medulla to dorsal horn Correct answer.
  3. Thalamus to cortex to dorsal horn
  4. Cerebellum to vestibular nuclei to spinal cord

Explanation

The periaqueductal gray projects to the rostral ventromedial medulla, which sends serotonergic and noradrenergic fibers to the dorsal horn. These fibers inhibit nociceptive transmission presynaptically and postsynaptically, and are engaged by opioids and by stress-induced analgesia.

Question 12Pain anatomy, physiology, and pharmacology

Visceral pain is frequently referred to somatic structures because of which arrangement?

  1. Visceral organs lack nociceptors
  2. Visceral afferents synapse in the ventral horn
  3. Visceral and somatic afferents converge on the same second-order neurons Correct answer.
  4. Somatic afferents are unmyelinated

Explanation

Convergence-projection holds that visceral and somatic afferents from the same spinal segment synapse on shared second-order neurons. The brain, more accustomed to somatic input, misattributes the source to the corresponding dermatome or myotome.

Question 13Pain anatomy, physiology, and pharmacology

Gabapentin reduces neuropathic pain by binding to which target?

  1. NMDA receptor glycine site
  2. Mu opioid receptor
  3. Cyclooxygenase-2
  4. Alpha-2-delta subunit of voltage-gated calcium channels Correct answer.

Explanation

Gabapentinoids bind the alpha-2-delta auxiliary subunit of presynaptic voltage-gated calcium channels. This reduces calcium influx and release of excitatory transmitters from hyperexcitable nociceptive terminals.

Question 14Pain anatomy, physiology, and pharmacology

At low subanesthetic doses, ketamine's antihyperalgesic effect is mediated mainly by which action?

  1. Sodium channel blockade
  2. GABA-A potentiation
  3. NMDA receptor antagonism Correct answer.
  4. COX-2 inhibition

Explanation

Ketamine is a noncompetitive antagonist at the phencyclidine site of the NMDA receptor. Blocking NMDA receptors reduces windup and central sensitization, which underlies its use in refractory and opioid-tolerant pain.

Question 15Pain anatomy, physiology, and pharmacology

Topical capsaicin produces initial burning followed by analgesia through which mechanism?

  1. Inhibition of substance P synthesis in the liver
  2. TRPV1 agonism with eventual defunctionalization of nociceptors Correct answer.
  3. Selective COX-2 inhibition
  4. Blockade of voltage-gated sodium channels

Explanation

Capsaicin activates the TRPV1 cation channel on C fibers, causing release of substance P and CGRP and producing the initial burning. Repeated exposure desensitizes and defunctionalizes these terminals, reducing later nociceptive signaling.

Question 16Pain anatomy, physiology, and pharmacology

Tramadol's analgesic effect combines weak mu opioid agonism with which additional action?

  1. GABA-A agonism
  2. Inhibition of serotonin and norepinephrine reuptake Correct answer.
  3. COX-2 inhibition
  4. NMDA antagonism

Explanation

Tramadol is a weak mu agonist whose metabolite formed by CYP2D6 contributes most of the opioid effect. It also inhibits serotonin and norepinephrine reuptake, adding descending inhibitory modulation but raising the risk of serotonin syndrome and seizures.

Question 17Pain anatomy, physiology, and pharmacology

A patient taking high-dose full-agonist opioids is transitioned to buprenorphine and develops acute withdrawal. Which property of buprenorphine best explains this?

  1. Partial mu agonism with high receptor affinity Correct answer.
  2. Pure kappa antagonism
  3. Irreversible cyclooxygenase inhibition
  4. Nonselective sodium channel blockade

Explanation

Buprenorphine binds mu receptors with high affinity but produces less intrinsic activity than full agonists. It therefore displaces the full agonist while providing lower receptor activation, precipitating withdrawal in a dependent patient.

Question 18Pain anatomy, physiology, and pharmacology

Intrathecal clonidine produces analgesia chiefly by activating which dorsal horn receptors?

  1. Alpha-2 adrenergic receptors Correct answer.
  2. GABA-B receptors
  3. TRPV1 channels
  4. Mu opioid receptors

Explanation

Alpha-2 adrenergic agonists inhibit presynaptic transmitter release and hyperpolarize postsynaptic dorsal horn neurons. Clonidine is used neuraxially for nociceptive and sympathetically maintained pain, with hypotension and bradycardia as expected adverse effects.

Question 19Pain anatomy, physiology, and pharmacology

A patient on a stable high-dose opioid reports worsening diffuse pain with spreading tenderness despite further dose escalation. Which phenomenon is most likely?

  1. Opioid-induced hyperalgesia Correct answer.
  2. Opioid tolerance
  3. Incomplete cross-tolerance
  4. Physical dependence

Explanation

Opioid-induced hyperalgesia is a paradoxical sensitization in which opioids increase pain sensitivity, producing diffuse pain and tenderness that worsens with higher doses. It differs from tolerance, in which the same nociceptive stimulus simply requires more drug for the same effect. Dose reduction or rotation may be required.

Question 20Pain anatomy, physiology, and pharmacology

Repetitive C-fiber stimulation that produces progressively larger dorsal horn responses (windup) requires activation of which receptor?

  1. Opioid receptor
  2. NMDA receptor Correct answer.
  3. Alpha-2 adrenergic receptor
  4. GABA-A receptor

Explanation

Windup reflects frequency-dependent summation of dorsal horn responses and depends on NMDA receptor activation after relief of the voltage-dependent magnesium block. This process contributes to central sensitization, secondary hyperalgesia, and allodynia.

Question 21Pain anatomy, physiology, and pharmacology

Which mechanism best explains sympathetically maintained pain in complex regional pain syndrome?

  1. Excess GABA release in lamina II
  2. Upregulation of adrenergic receptors on nociceptors Correct answer.
  3. Selective loss of A-beta fibers
  4. Increased mu receptor density on motor neurons

Explanation

After nerve injury, nociceptive neurons can develop adrenergic sensitivity, and sympathetic fibers may sprout into the dorsal root ganglion. Sympathetic outflow and norepinephrine then enhance nociceptor firing, producing pain that responds to sympathetic blockade.

Question 22Pain anatomy, physiology, and pharmacology

Which agent used intrathecally for refractory severe pain is a conopeptide that blocks N-type voltage-gated calcium channels?

  1. Baclofen
  2. Morphine
  3. Ziconotide Correct answer.
  4. Bupivacaine

Explanation

Ziconotide binds Cav2.2 N-type calcium channels on primary afferent terminals, blocking release of substance P and glutamate. It is a nonopioid analgesic delivered by intrathecal pump and can cause psychiatric and cognitive adverse effects.

Question 23Pain anatomy, physiology, and pharmacology

Tanezumab and related monoclonal antibodies developed for chronic pain target which mediator?

  1. Nerve growth factor Correct answer.
  2. Tumor necrosis factor-alpha
  3. Interleukin-6
  4. Calcitonin gene-related peptide

Explanation

Nerve growth factor released by injured or dysfunctional tissue sensitizes nociceptors through TrkA signaling. Sequestration of NGF reduces nociceptor sensitization, although trials raised concern about rapid joint destruction in osteoarthritis.

Question 24Pain anatomy, physiology, and pharmacology

Which opioid carries the greatest risk of serotonin syndrome when combined with an SSRI?

  1. Fentanyl
  2. Oxycodone
  3. Meperidine Correct answer.
  4. Hydromorphone

Explanation

Meperidine inhibits serotonin reuptake and is the classic opioid associated with serotonin syndrome when combined with serotonergic drugs. Tramadol, methadone, and fentanyl also have serotonergic properties, but meperidine carries the highest risk.

Question 25Pain anatomy, physiology, and pharmacology

Wide dynamic range neurons in lamina V are important in pain processing because they do what?

  1. Release acetylcholine onto lower motor neurons
  2. Transmit only proprioceptive information to the cerebellum
  3. Are located within the dorsal root ganglion
  4. Receive both innocuous A-beta and nociceptive A-delta/C input and encode intensity Correct answer.

Explanation

Wide dynamic range neurons receive convergent input from low-threshold mechanoreceptors and nociceptors, so their firing rate encodes stimulus intensity across a broad range. Their convergence properties underlie referred pain and contribute to secondary hyperalgesia after sensitization.

Question 26Pain anatomy, physiology, and pharmacology

A patient describes a sharp, well-localized pain immediately after touching a hot stove, followed by a dull, aching pain. The immediate sharp sensation is transmitted primarily by which fibers?

  1. Preganglionic sympathetic fibers
  2. Unmyelinated C fibers
  3. Myelinated A-delta fibers Correct answer.
  4. Large myelinated A-beta fibers

Explanation

A-delta fibers are thinly myelinated and conduct rapidly, so they mediate the fast, sharp first pain that is well localized. C fibers are unmyelinated and slower, producing the delayed dull, aching second pain.

Question 27Pain anatomy, physiology, and pharmacology

Which cortical region is most consistently associated with the affective-motivational dimension of pain rather than with sensory-discriminative localization?

  1. Primary motor cortex
  2. Primary somatosensory cortex
  3. Anterior cingulate cortex Correct answer.
  4. Cerebellar cortex

Explanation

Primary somatosensory cortex encodes the location and intensity of a noxious stimulus, whereas the anterior cingulate cortex and insula contribute strongly to the unpleasantness and emotional response to pain. Motor and cerebellar cortex are not primary pain-processing regions.

Question 28Pain anatomy, physiology, and pharmacology

Which agent reverses opioid-induced respiratory depression by competitively antagonizing mu opioid receptors?

  1. Atropine
  2. Flumazenil
  3. Neostigmine
  4. Naloxone Correct answer.

Explanation

Naloxone is a short-acting competitive opioid receptor antagonist that rapidly reverses mu-mediated effects such as respiratory depression and sedation. Flumazenil antagonizes benzodiazepines, whereas atropine and neostigmine act at muscarinic and cholinergic sites.

Question 29Pain anatomy, physiology, and pharmacology

Sumatriptan relieves acute migraine chiefly by activating which receptors?

  1. 5-HT1B/1D receptors Correct answer.
  2. Dopamine D2 receptors
  3. Alpha-1 adrenergic receptors
  4. GABA-A receptors

Explanation

Triptans are serotonin agonists with selectivity for 5-HT1B and 5-HT1D receptors, which promote cranial vasoconstriction and inhibit trigeminal neuropeptide release. Dopamine, GABA-A, and alpha-1 receptors are not the primary targets for triptan efficacy.

Question 30Pain anatomy, physiology, and pharmacology

Intrathecal morphine produces profound analgesia mainly through activation of which receptors in the dorsal horn?

  1. Kappa opioid receptors
  2. Mu opioid receptors Correct answer.
  3. Nicotinic acetylcholine receptors
  4. Delta opioid receptors

Explanation

Mu opioid receptors are densely expressed on primary afferent terminals and dorsal horn neurons, where intrathecal morphine reduces transmitter release and neuronal excitability. Kappa and delta receptors contribute to opioid biology but are not the principal target for morphine analgesia.

Question 31Pain anatomy, physiology, and pharmacology

Celecoxib provides analgesia with less gastric mucosal injury than ibuprofen primarily because it selectively inhibits which enzyme?

  1. Lipoxygenase
  2. COX-1
  3. Phospholipase A2
  4. COX-2 Correct answer.

Explanation

Celecoxib is a selective COX-2 inhibitor, sparing the constitutive COX-1 activity that supports gastric mucosal protection. Ibuprofen inhibits both isoforms and therefore carries greater gastrointestinal risk.

Question 32Pain anatomy, physiology, and pharmacology

A patient with ultrarapid CYP2D6 metabolism takes codeine and develops excessive sedation and respiratory depression. Which explanation is most likely?

  1. Codeine directly activates mu receptors with high affinity
  2. Codeine is converted more rapidly to morphine Correct answer.
  3. Codeine is converted to an inactive metabolite that blocks naloxone
  4. Codeine accumulates because CYP2D6 is saturated

Explanation

Codeine is a prodrug that undergoes CYP2D6-mediated O-demethylation to morphine, so ultrarapid metabolizers form excessive morphine and risk opioid toxicity. Poor metabolizers form less morphine and may obtain inadequate analgesia.

Question 33Pain anatomy, physiology, and pharmacology

Orthostatic hypotension during amitriptyline therapy is best attributed to blockade of which receptor?

  1. Serotonin 5-HT2 receptors
  2. Histamine H1 receptors
  3. Alpha-1 adrenergic receptors Correct answer.
  4. Muscarinic acetylcholine receptors

Explanation

Amitriptyline blocks alpha-1 adrenergic receptors, impairing compensatory vasoconstriction and producing orthostatic hypotension. Its muscarinic, histamine, and serotonin receptor effects explain other adverse effects such as dry mouth, sedation, and weight gain.

Question 34Pain anatomy, physiology, and pharmacology

After a peripheral tissue injury, which mediator directly lowers the activation threshold of nociceptors and contributes to primary hyperalgesia?

  1. Prostaglandin E2 Correct answer.
  2. Acetylcholine
  3. Dopamine
  4. GABA

Explanation

Inflammatory mediators such as prostaglandin E2 sensitize nociceptor terminals by acting on G-protein-coupled receptors that increase cAMP and reduce the threshold for firing. This peripheral sensitization contributes to tenderness and hyperalgesia at the injury site.

Question 35Pain anatomy, physiology, and pharmacology

Buprenorphine's ceiling effect on respiratory depression is best explained by which pharmacologic property?

  1. Full agonism at delta opioid receptors
  2. Competitive antagonism at kappa opioid receptors
  3. Irreversible inhibition of opioid metabolism
  4. Partial agonism at mu opioid receptors Correct answer.

Explanation

Buprenorphine binds mu opioid receptors with high affinity but produces submaximal activation, so dose escalation yields progressively less additional respiratory depression. This partial agonism underlies its ceiling effect and its utility in selected pain and addiction settings.

Question 36Pain anatomy, physiology, and pharmacology

Tapentadol differs from pure mu opioid agonists in that it also produces analgesia by which action?

  1. Inhibiting cyclooxygenase-2
  2. Inhibiting norepinephrine reuptake Correct answer.
  3. Blocking voltage-gated sodium channels
  4. Activating GABA-B receptors

Explanation

Tapentadol combines mu opioid receptor agonism with inhibition of norepinephrine reuptake, enhancing descending inhibitory control. This dual mechanism distinguishes it from pure mu agonists and contributes to its use in neuropathic and mixed pain states.

Question 37Pain anatomy, physiology, and pharmacology

During induction of spinal anesthesia, which modality is typically lost first as the block ascends?

  1. Light touch
  2. Sympathetic vasomotor tone Correct answer.
  3. Motor strength
  4. Proprioception

Explanation

Small unmyelinated sympathetic fibers are most susceptible to local anesthetic blockade, so vasomotor tone is lost before pain and temperature sensation. Light touch, proprioception, and motor function are lost at progressively higher block levels.

Question 38Pain anatomy, physiology, and pharmacology

A child has episodes of burning distal extremity pain, erythema, and elevated skin temperature from infancy. Gain-of-function mutations in which channel are most likely responsible?

  1. Kv1.1 potassium channel
  2. Nav1.5 sodium channel
  3. Nav1.7 sodium channel Correct answer.
  4. TRPM8 menthol receptor

Explanation

Nav1.7 is highly expressed in dorsal root ganglion nociceptors, and gain-of-function mutations lower the firing threshold, producing inherited erythromelalgia with burning pain and erythema. Nav1.5 is primarily cardiac, Kv1.1 is linked to episodic ataxia, and TRPM8 is a cold-sensing receptor.

Question 39Pain anatomy, physiology, and pharmacology

A patient with chronic kidney disease receiving high-dose morphine develops myoclonus and hyperalgesia. Accumulation of which metabolite is most implicated?

  1. Morphine-6-glucuronide
  2. Normorphine
  3. Morphine-3-glucuronide Correct answer.
  4. Codeine

Explanation

Morphine-3-glucuronide is renally cleared and accumulates in kidney disease, where it can produce neuroexcitation, myoclonus, and hyperalgesia. Morphine-6-glucuronide is analgesic and can cause respiratory depression but is not the metabolite most associated with these excitatory effects.

Question 40Pain anatomy, physiology, and pharmacology

Which ascending pathway relays nociceptive information to the amygdala and is most implicated in the emotional-affective component of pain?

  1. Dorsal column-medial lemniscus pathway
  2. Corticospinal tract
  3. Spinoparabrachial pathway Correct answer.
  4. Spinothalamic tract to the ventroposterolateral nucleus

Explanation

The spinoparabrachial pathway projects to the parabrachial nucleus and then to the amygdala and other limbic structures, contributing to the affective and aversive dimension of pain. The spinothalamic projection to the ventroposterolateral nucleus supports sensory-discriminative processing instead.

Question 41Evaluation and diagnosis of painful conditions

A patient describes sharp, lancinating pain that travels from the buttock down the posterior thigh into the lateral calf, and the pain is reproduced by straight leg raising. Which mechanism best accounts for this presentation?

  1. Somatic nociceptive pain from lumbar paraspinal muscle strain
  2. Referred visceral pain of renal origin
  3. Nociplastic pain from central sensitization
  4. Radicular pain from nerve root irritation Correct answer.

Explanation

Electric, lancinating pain in a dermatomal distribution that is reproduced by nerve-root tension maneuvers is the hallmark of radicular pain, which is neuropathic in mechanism. Somatic nociceptive pain is typically dull and achy and is not reproduced by straight leg raising.

Question 42Evaluation and diagnosis of painful conditions

A patient cannot extend the great toe against resistance and has reduced sensation over the dorsum of the foot and the first web space. This most specifically localizes the lesion to which nerve root?

  1. L4
  2. L5 Correct answer.
  3. S1
  4. S2

Explanation

L5 supplies the extensor hallucis longus and provides sensation to the dorsum of the foot including the first web space. L4 lesions affect the quadriceps and patellar reflex, while S1 lesions affect plantar flexion and the lateral foot.

Question 43Evaluation and diagnosis of painful conditions

A patient reports nighttime numbness and tingling of the thumb, index, and middle fingers that is relieved by shaking the hand. Which provocative maneuver best supports the suspected diagnosis?

  1. Phalen test Correct answer.
  2. McMurray test
  3. Cozen test
  4. Finkelstein test

Explanation

Nocturnal paresthesias in the median nerve distribution with relief by shaking suggest carpal tunnel syndrome, and the Phalen wrist-flexion test is designed to reproduce it. Finkelstein tests the first dorsal extensor compartment, Cozen the lateral elbow, and McMurray the meniscus.

Question 44Evaluation and diagnosis of painful conditions

A patient with neck pain and electric pain radiating into the right arm is being examined. Which maneuver is most useful for reproducing cervical nerve root compression?

  1. Bakody sign
  2. Lhermitte sign
  3. Adson test
  4. Spurling test Correct answer.

Explanation

The Spurling maneuver extends, side-bends, and rotates the neck to narrow the cervical neural foramen, reproducing radicular symptoms with high specificity. Adson testing evaluates thoracic outlet compression, Lhermitte reflects dural or posterior column irritation, and the Bakody sign relieves rather than provokes radicular pain.

Question 45Evaluation and diagnosis of painful conditions

Which examination finding best supports the sacroiliac joint as the source of a patient's unilateral low back and buttock pain?

  1. Three or more positive SI provocation maneuvers Correct answer.
  2. A single positive FABER test
  3. Pain reproduced by lumbar extension only
  4. A positive straight leg raise at 30 degrees

Explanation

Because individual sacroiliac provocation tests are imprecise, a cluster of three or more positive maneuvers (distraction, compression, thigh thrust, Gaenslen, sacral thrust) is used to support the joint as the source. Single tests, including FABER, are sensitive but poorly specific.

Question 46Evaluation and diagnosis of painful conditions

A 72-year-old presents with two weeks of bilateral shoulder and hip girdle aching and morning stiffness lasting 90 minutes, without peripheral joint swelling. Which diagnosis is most likely?

  1. Rotator cuff tendinopathy
  2. Fibromyalgia
  3. Polymyalgia rheumatica Correct answer.
  4. Rheumatoid arthritis

Explanation

New bilateral girdle pain with prolonged morning stiffness in an older adult, without peripheral synovitis, is the classic presentation of polymyalgia rheumatica, and inflammatory markers are usually markedly elevated. Fibromyalgia does not elevate acute-phase reactants and typically causes widespread pain rather than girdle-limited stiffness.

Question 47Evaluation and diagnosis of painful conditions

Which set of findings is required to diagnose complex regional pain syndrome using the Budapest criteria?

  1. Disproportionate pain plus at least one sign and one symptom in two or more categories Correct answer.
  2. A documented peripheral nerve injury together with increased radiotracer uptake on a three-phase bone scan
  3. Objective motor weakness together with a sustained response to a diagnostic sympathetic ganglion block
  4. Allodynia in a stocking distribution together with elevated erythrocyte sedimentation rate and C-reactive protein

Explanation

The Budapest criteria require continuing pain disproportionate to any inciting event, at least one symptom in two or more of the four categories (sensory, vasomotor, sudomotor/edema, motor/trophic), and at least one sign in two or more categories at examination, with no better explanation. A discrete nerve injury is neither required nor excluded, which is how CRPS type II is distinguished from type I.

Question 48Evaluation and diagnosis of painful conditions

Which questionnaire is designed to screen for a neuropathic pain component in a patient with chronic pain?

  1. painDETECT Correct answer.
  2. Widespread pain index
  3. Oswestry Disability Index
  4. Patient Health Questionnaire-9

Explanation

painDETECT, like DN4 and LANSS, screens for neuropathic descriptors such as burning, electric shocks, and evoked pain. The widespread pain index quantifies fibromyalgia pain distribution, the Oswestry index measures disability, and the PHQ-9 screens for depression.

Question 49Evaluation and diagnosis of painful conditions

A patient with acute low back pain reports new urinary retention and numbness of the perineum and inner thighs. What is the most appropriate next step?

  1. Reassurance and a trial of NSAIDs
  2. Emergent MRI of the lumbosacral spine Correct answer.
  3. Outpatient physical therapy with follow-up in six weeks
  4. Lumbar epidural steroid injection

Explanation

Saddle anesthesia with bladder dysfunction indicates possible cauda equina syndrome, which is a surgical emergency. Urgent imaging and neurosurgical consultation are required because delays can produce permanent sphincter and sensory deficits.

Question 50Evaluation and diagnosis of painful conditions

Which feature of back pain is most suggestive of an inflammatory spondyloarthropathy rather than a mechanical cause?

  1. Pain that is always unilateral and sharp
  2. Pain that is worse with activity and relieved by rest
  3. Morning stiffness lasting more than 30 minutes that improves with exercise Correct answer.
  4. Pain that begins after age 50

Explanation

Inflammatory back pain features insidious onset before age 40, prolonged morning stiffness that improves with activity, and night pain that eases with movement. Mechanical pain typically worsens with activity and improves with rest.