Chronic Pain
Christopher J. Gilligan
Aditi Malhotra
Kiran V. Patel
BACKGROUND
Definitions
1. Pain is a learned unpleasant sensory and emotional experience associated with, or resembling that which is associated with, actual or potential tissue damage.
2. Chronic pain is long-standing pain that persists beyond the normal healing period of 3 months or occurs along with a chronic health condition, such as arthritis.
3. Allodynia is pain caused by a stimulus that does not normally provoke pain.
4. Analgesia is a state of reduced sensibility to pain in response to a stimulus that would normally cause pain.
5. Paresthesia is an abnormal sensation, described as a burning, prickling, or numbness, felt in any part of the body whether spontaneous or evoked.
6. Hyperalgesia is a state of increased sensitivity to feeling pain or extreme response to pain from a stimulus that does or does not normally provoke pain.
7. Primary hyperalgesia is increased pain around tissue injury, typically caused by peripheral sensitization.
8. Secondary hyperalgesia is increased pain beyond the anatomical area of injury, typically caused by central sensitization.
9. Temporal summation is an increasing sensation of pain due to the application of a repetitive and equal stimulus over a brief period, typically caused by central sensitization.
10. Peripheral sensitization is a reduction in pain threshold and/or increased responsiveness at peripheral nerve endings and sensory nerve fibers at the site of tissue damage, often resulting in primary hyperalgesia.
11. Central sensitization is the increased responsiveness of nociceptive neurons in the central nervous system (CNS) to their normal or subthreshold afferent inputs, caused by increases in membrane excitability and synaptic efficacy.
12. Nociceptors are high-threshold primary sensory neurons, which run in thinly myelinated A-δ and unmyelinated C-fibers. Transducing ion channels enable them to sense noxious stimuli, which can be mechanical, thermal, or chemical, causing damage to the body’s integrity.
Epidemiology
1. Pain affects more Americans than diabetes, heart disease, and cancer combined. Chronic pain is estimated to afflict about 21% (51.6 million persons) of the US population.
2. About 6.9% (17.1 million persons) of the US population experiences high-impact chronic pain, meaning it causes substantial restrictions to daily activities.
3. Pain is the most common reason Americans access the health care system and is the most common cause of long-term disability, lost productivity, and increased health care costs.
4. The most common pain conditions are chronic low back pain, neck pain, pelvic pain, diabetic peripheral neuropathic pain, and headaches, followed by large joint pain (hip, knee, shoulder), and to a lesser degree hand/wrist and ankle/foot pain as well as abdominal pain.
5. Most chronic pain conditions are more common in females than in males.
6. Prevalence of headaches peaks around an age of 30 years, whereas most other chronic pain conditions have increased prevalence with age, mostly because of arthritic conditions.
7. At least 50% of patients with cancer have chronic pain as a prominent symptom of their disease, and these numbers increase for certain cancer types, locations (eg, head/neck cancer), and advanced stages, in which pain control often becomes the focus of clinical management.
Classification
1. Pain can be classified according to its anatomical location, pathologic state, or underlying cellular mechanisms.
a. In clinical practice, there is a strong emphasis on anatomical location (eg, low back pain caused by facet joint disease, disc disease, muscle spasms) especially among surgical and interventional specialties.
b. Identifying distinct pathologic pain states can be challenging because they often coexist. For example, a herniated disc can cause changes in mechanical joint pressure (nociceptive pain), an inflammatory response in the surrounding tissue (inflammatory pain), as well as compression/damage to the nerve root (neuropathic pain).
c. Cellular mechanisms are currently nearly impossible to detect clinically, except in distinct genetic pain conditions and possibly by elaborate quantitative sensory testing.
Anatomical Classification (Exemplified by Pain of Spine Origin)
1. Facet joint disease: Osteoarthrosis, osteoarthritis (secondary to degenerative changes or underlying rheumatologic disease), facet cyst
2. Disc disease: Degenerative disc disease, disc herniation
3. Bone disease: Caused by fracture or neoplasm
4. Nerve root disease: Compression by herniated disc, bone (bone spur, antero- or retrolisthesis), facet cyst, or muscle spasm (eg, piriformis syndrome); infiltration by neoplasm; immune-mediated inflammation (eg, diabetic radiculoplexus neuropathy, chronic inflammatory demyelinating disease [CIDP])
5. Myofascial pain
Pathologic State
1. Nociceptive pain is caused by activation of nociceptors (high-threshold primary sensory neurons) by intense, typically in the case of clinical pain, mechanical stimuli.
a. Examples include:
1) Deep somatic nociceptive pain is caused by increased mechanical forces (eg, joint capsule stretch) on spinal discs because of degenerative destruction of facet joints, nerve impingements.
2) Superficial somatic nociceptive pain includes skin damage from trauma, chemical stimuli, thermal stimuli, and irritation of mucous membranes.
2. Inflammatory pain is caused by activation and sensitization of nociceptors by inflammatory mediators. Clinically, there is often an interplay between mechanical irritation and subsequent inflammation.
a. Tissue damage or inflammation results in release of inflammatory signaling molecules from local immune cells (eg, prostaglandins, cytokines). These agents can either directly activate transducing ion channels at nociceptor endings or sensitize them, resulting in a lower activation threshold and increased responsiveness to stimuli.
b. Ongoing inflammation can result in longer-lasting changes of trafficking, cell surface expression, and gating properties of the nociceptive ion channels.
c. Ongoing peripheral inflammation induces changes in the affected spinal segments, as well as higher brain areas, via systemically activating cytokines such as IL-1β, resulting in anatomically more widespread pain and pain triggered by several different stimuli (mechanical, thermal, etc.).
d. Examples of inflammatory pain include:
1) Osteoarthritis is joint degeneration (osteoarthrosis), which can result in an inflammatory immune response, leading to further destruction of the joint and, eventually, chronic inflammation. Most common joints affected are knee, hip, facet joints, and hands.
2) Primary/autoimmune synovitis, as seen in rheumatologic arthritides (eg, rheumatoid arthritis), is where the primary event is an autoimmune inflammation of the synovia, resulting in synovial hyperplasia, joint destruction, and systemic inflammatory symptoms.
3) Disc herniation is the release of the immunogenic nucleus and other disc material into proximity of the nerve root, causing local inflammation of the root and adjacent structures.
4) Inflammatory diseases of the visceral organs, for example, cholecystitis, inflammatory bowel disease, tumor infiltration.
5) Infection causing secondary, immune-mediated inflammation. In addition, certain gram-negative and gram-positive bacteria can directly activate nociceptive receptors via specific surface antigens.
3. Neuropathic pain is caused by damage to the sensory components of the nervous system, in either the peripheral or central nervous system.
a. Peripheral neuropathic pain is caused by damage to the peripheral nerves, plexus, or roots.
1) Systemic diseases, toxicities, or deficiency states typically cause a polyneuropathy or mononeuritis multiplex, whereas a focal process results in a mononeuropathy/radiculopathy.
2) The etiology of neuropathic pain is manyfold: Nerve damage/cut (eg, postmastectomy pain syndrome, postinguinal hernia repair pain), mechanical compression (eg, entrapment neuropathies), ischemia (eg, because of vasculitis or diabetes), axonal degeneration because of systemic disease (alcohol, diabetes), demyelination (CIDP), and postinfectious (postherpetic neuralgia).
3) In many neuropathic pain conditions, there is an element of peripheral inflammation that drives the sensitization of the affected nerve/root: root inflammation from ruptured disc, postsurgical inflammation, mechanical nerve compression, autoimmune inflammation as in CIDP.
4) Neuroma is a tangled mass of regenerating axons embedded within nerve connective tissue, which often develop after traumatic nerve severance or amputation (stump neuroma). Changes in nociceptive nerve fiber phenotype with upregulation of sodium channels cause these nerve bundles to show abnormal electrical hyperexcitability and cause spontaneous as well as easily provoked neuropathic pain.
b. Central neuropathic pain occurs because of pathology disrupting nociceptive processing anywhere along the CNS. The pathology of the lesion is less important than its anatomical location. Damage to the nerve root entry zone, the spinothalamic tract (STT), and/or the sensory thalamus by any process can result in central neuropathic pain.
1) Common conditions include ischemic and hemorrhagic stroke, brain or spinal cord tumor or trauma, spinal syringomyelia, demyelination because of multiple sclerosis, and acute disseminated encephalomyelitis.
2) For central poststroke pain (CPSP), see later in this chapter.
Pain Mechanisms
1. Nociception
a. Pain-sensing neurons (nociceptors) feature specialized receptors (transducers) at their nerve endings that translate specific stimuli into membrane depolarization. Transducer examples include the ligand and heat-gated TRPV1 (heat, capsaicin), TRPM8 (cold, menthol), TRPA1 (allicin), acid-sensing ion channels for free protons, and Piezo2 (mechanical stimulus).
b. When specific stimuli are present at their respective transducers, voltage-gated sodium channels (eg, Nav1.7, Nav1.8, and Nav1.9) are activated, depolarizing the nociceptive neurons and firing an action potential. Sodium channels can amplify the initial signal by various mechanisms, encoding the initial stimulus intensity into action potential frequency. Depending on their activation thresholds, these sodium channels can determine the excitability of nociceptors.
1) Mutations in the expression and binding properties of these sodium channels can cause the neuron to have absence of or abnormal firing patterns, leading to the development of neuropathic pain. As an example, a rare Nav1.7 mutation can cause either complete inability to sense pain or intense, intermittent pain attacks, known as erythromelalgia.
2. Pain pathways
a. Myelinated A-δ and unmyelinated C-fibers are major contributors to localized sharp and slow and poorly localized nociception, respectively. A-β fibers contribute to pathologic states of central sensitization, causing mechanical allodynia.
b. Ascending pain pathway
1) Activation of nociceptors results in the emission of glutamate and peptides from first-order neurons within the dorsal horn of the spinal cord (mostly superficial laminae LI and LII with some projections to LV). First-order neurons then release substance P, a critical neurotransmitter for pain transmission, and synapse on second-order neurons in the dorsal horn. Second-order neurons cross the midline to the contralateral side of the spinal cord and traverse toward the brain, forming the ascending STT. Modulated afferent information is transmitted up via the anterior and lateral STT and
synapses on the third and final neuron of the ascending pathway, the ventral posterior lateral (VPL) subnucleus of the thalamus. The axons from the VPL project to the primary somatosensory cortices (SM1, SM2), transmitting sensations of pain, temperature, and itch from the contralateral side of the body to the brain for further processing.
c. Descending pain pathway
1) Neurons in this pathway originate in the periaqueductal gray (PAG) matter of the midbrain and project to the serotoninergic nucleus raphe of the medulla and then the norepinephrinergic locus coeruleus. This pathway can modulate incoming afferents at the dorsal horn level.
2) Axons from the PAG project mainly to superficial spinal laminae (LI and LII) in the dorsal horn and inhibit communication between the primary- and secondary-order neurons of the ascending pathway via γ-aminobutyric acid (GABA) and glycine-releasing central projection neurons, filtering and dampening pain signals from reaching the brain.
3) Further modulation of incoming signals is mediated by a complex network of inhibitory and excitatory spinal interneurons.
d. Trigeminothalamic axons from the spinal nucleus of the trigeminal nerve decussate to the contralateral STT to convey equivalent sensations from the face to the ventral posterior medial subnucleus in the thalamus.
e. Other nociceptive projections include collaterals to different thalamic nuclei:
1) The posterior ventral medial nucleus (VMpo) further projects to the posterior insula, where information is integrated with visceral afferent activity (eg, vagal and gustatory afferents) to influence autonomic responses.
2) The medial dorsal nucleus (MDvc) relays information to the anterior cingulate cortex and is important for the affective/motivational aspect of pain.
3) The intralaminar thalamic nuclei have widespread cortical projections contributing to arousal and attention.
3. Peripheral sensitization
a. Peripheral sensitization is a decreased depolarization threshold and/or increased responsiveness of nociceptors because of posttranslational changes and altered trafficking of transducer receptors (eg, TRPV1) and voltage-gated ion channels (eg, Nav channels).
b. These changes are typically driven by inflammatory molecules (eg, bradykinin, histamine, prostaglandins, nerve growth factor) resulting in phosphorylation and therefore sensitization of transducers and upregulation of sodium channels.
c. Clinically, the decreased depolarization threshold coupled with the upregulation of sodium channels and the influx of ions causes an increase in the firing of action potentials. The firing results in pain (especially thermal) hypersensitivity confined to the inflamed area (zone of primary hyperalgesia). If these alterations to the nociceptors are longer lasting, they can cause changes in the neuron expression patterns.
4. Central sensitization
a. Central sensitization is an increased responsiveness of nociceptive neurons in the CNS to normal or subthreshold afferent input. This occurs in pain of both peripheral and central origin and often coexists with peripheral sensitization.
b. Activity-dependent mechanisms (ie, driven by ongoing peripheral afferent activity) include:
1) Homosynaptic potentiation, which is the strengthening of the synapse between the nociceptor and dorsal horn projection neuron. Clinically results in temporal summation.
2) Heterosynaptic potentiation is the strengthening of synapses between other, nonnociceptive afferents (eg, Aβ fibers) and dorsal horn projection neurons. Low-threshold Aβ fibers (sensing, eg, light touch) get to be recruited into the pain pathway, resulting in mechanical allodynia as well as pain hypersensitivity outside the primary affected area (zone of secondary hyperalgesia).
c. Spinal disinhibition of central projection neurons is caused by decreased GABAergic and glycinergic tone, causing an increased transmission of pain signals to the brain from the periphery.
1) Mechanisms include reduced descending inhibitory control, loss of GABAergic and glycinergic interneurons through cell death (eg, after peripheral nerve trauma), reduced GABA levels, and altered properties of GABAA and glycinergic receptors.
d. Central inflammation occurs after peripheral nerve injury and is driven by:
1) Neuronally derived mediators activating spinal microglia, which then release molecules causing astrogliosis and invasion of T cells into the spinal cord.
2) The further release of immune mediators from microglia enhances synaptic neurotransmission by increasing glutamate release as well as α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor modulation. Astrocytes contribute to increased synaptic glutamate levels by downregulation of spinal astrocyte glutamate transporters.
e. Brain changes in chronic pain include (partially reversible) decrease in neocortex gray matter, changes in excitatory and inhibitory transmitters, and changes in functional connectivity of pain-sensing brain areas.
5. The biopsychosocial model
a. The relationship between the nociceptive stimulus (“disease”) and the degree of pain reported or pain-related behaviors (“illness”) depends on biologic, psychological, and social factors.
b. The level of suffering and the affective and behavioral expression of pain are mediated by cognitive reactions to the nociceptive stimulus and its environmental context (eg, cancer pain engenders fear and exaggerates the experience of pain).
c. Although the nociceptive component can often not be cured, the affective reaction and behavior can be modulated to reduce disability.
d. Management of chronic pain requires that the treating physician incorporates the multidimensional nature of the pain experience and takes a holistic approach to treatment via adjusted treatments, psychological therapies, and lifestyle modification and advises accordingly.
Diagnosis
1. As with any medical specialty, treatment is most impactful if it is geared toward a specific pathology. The goal is to identify a specific anatomical location and/or underlying mechanism of pain generation, which is often difficult to do with certainty.
2. Medical diagnosis is hampered by low specificity of subjective symptoms and physical examination signs, as well as the poor correlation of imaging findings
and symptoms. There is no gold standard to diagnosing the cause of chronic pain.
3. Along the lines of the biopsychosocial construct, modulating psychological (both affective and cognitive) factors and behaviors can often result in reduced disability and should be evaluated.
4. It is important to adjust patient expectations toward pain reduction/management and to define goals by functional improvement rather than absolute pain scores. The relentless pursuit of a “definitive” diagnosis is discouraged unless worrisome systemic symptoms or progressive neurologic deficits exist.
Pain Assessment
1. Pain characteristics include:
a. Pain location: focal, radiating, referred, multifocal/whole body
b. Severity: best to evaluate range (least to worst); several scales can be used:
1) Numeric rating scale (0-10, 0-20, or 0-100)
2) Verbal rating scale (eg, mild, moderate, severe, horrible, excruciating)
3) Visual analog scale (VAS) (eg, using drawn faces of pain expression)
c. Quality of pain (nonspecific, best validated for neuropathic pain)
1) Characteristics of neuropathic pain (based on pain questionnaires): mechanical and temperature-evoked allodynia, numbness to several modalities, burning/tingling/electric, shock-like paresthesia, absence of persistent pain, and presence of intermittent pain attacks.
2) There are no specific symptoms of nociceptive or inflammatory pain.
3) Typically, several pain states coexist in any given condition.
d. Temporal profile and frequency: intermittent/paroxysmal, continuous
e. Modulating factors: precipitating, aggravating, and relieving pain
f. Neurologic deficits: changes in tone, involuntary movements or posturing, weakness, paresthesia, numbness, disequilibrium, neuraxial symptoms like bowel and bladder incontinence
g. Autonomic features: changes in color, temperature, sweating, trophic changes (skin, hair growth, nails)
h. Symptoms suggestive of more serious systemic pathology: progressive severity/location/neurologic deficit, weight loss, fever, malaise, skin rashes
2. Structured assessments of pain characteristics can be done using pain questionnaires: McGill Pain Questionnaire or the Brief Pain Inventory. Correlation to specific pathology or impact on treatment choices is uncertain. The Oswestry Disability Index (ODI) can be used to measure how a patient’s lower back pain impacts their ability to do daily tasks and activities.
3. Great efforts have been made to identify symptom clusters to identify subgroups of patients who share common pathology and might respond to a certain treatment. Commonly used and validated pain questionnaires focus on identifying patients with neuropathic pain/neuropathic components and are available in several languages: Douleur Neuropathique 4 (DN4), Neuropathic Pain Questionnaire (NPQ), and painDETECT questionnaire.
Pain-Related Assessment
1. The affective presentation and psychiatric diseases such as anxiety, depression, and posttraumatic stress disorder (PTSD) can play a major role in the patient’s disability and should be explored. Useful questionnaires include the Beck Anxiety Inventory, the Beck Depression Inventory, and the Center for Epidemiological Studies-Depression Scale.
2. Behavioral assessment should include evaluation of recent doctor/emergency room visits, pain-specific behaviors (eg, guarding, moaning), and impairment of activities of daily life and social interactions.
3. The cognitive perception of pain is an important modulator of the pain experience. Beliefs that activity-induced pain causes more damage, that pain controls one’s life (helplessness), that a serious illness is the cause of pain, or that pain is catastrophizing results in higher disability and should be treated with cognitive behavioral therapy (CBT).
a. The Pain Catastrophizing Scale is a tool to measure the beliefs and thoughts associated with an individual’s lower back pain experience, where a high score indicates higher level of catastrophic thoughts. It is a 13-item self-report questionnaire where patients are asked to rate the degree to which they have certain thoughts on a 4-point Likert scale, specifically associated with lower back pain.
4. Psychosocial variables including relationships, work environment, and social support, as well as presence of litigation and spiritual attitudes, can all influence the patient’s pain experience.
Physical Signs in the Examination of the Patient With Chronic Pain
1. A targeted musculoskeletal and neurologic examination should be performed. While many physical examination findings are too unspecific to point toward a specific pain generator, they are most valuable to exclude dangerous conditions.
2. Important physical signs include:
a. Sensation: Diminished or absent sensibility to primary sensory modalities, including small fiber (pinprick and temperature) and large fiber (vibration and position sense) modalities. The anatomical distribution of these deficits can follow bilateral symmetric versus peripheral nerve versus dermatomal.
b. Pain: Increased pain to noxious stimuli in a defined anatomical distribution (eg, nerve, dermatome, joint) indicates peripheral sensitization and is termed primary hyperalgesia. Pain beyond the anatomical location of a disease process (secondary hyperalgesia) as well as mechanical allodynia and temporal summation (see section on Definitions) indicate central sensitization.
c. Weakness: Anatomical distribution of weakness (symmetric vs peripheral nerve vs myotome) and focal/symmetric loss of reflexes.
d. Neuraxial symptoms: Sensory trunk level, increased tone/spasticity (if chronic), Babinski sign, and incontinence.
e. Cranial nerve findings: Including optic disc visualization (particularly important for head/neck pain).
f. Autonomic findings: Vasomotor (swelling, color, and temperature changes) and sudomotor (sweating) changes. Particularly important for diagnosing autonomic/small fiber neuropathies and complex regional pain syndrome (CRPS).
g. Physical maneuvers (all hampered by lack of gold standard to determine sensitivity and specificity of the maneuver).
1) Straight leg (high sensitivity) and crossed straight leg raise (high specificity) tests are indicative of a lumbar radiculopathy or sciatic nerve disease.
2) Spurling test (laterally flexing, rotating, and compressing the patient’s head toward the symptomatic side), traction/neck distraction, and the Valsalva maneuver might be suggestive of a cervical radiculopathy (higher specificity), while a negative upper limb traction test might be used to rule it out (higher sensitivity).
3) Musculoskeletal palpation and manipulation of the spine as well as provocative tests for facetogenic and sacroiliac pain show poor diagnostic validity and interobserver reliability.
Special Pain Syndromes
1. Centralized pain
a. Centralized pain syndrome is an umbrella term for chronic, often widespread, pain conditions, where there is no noxious stimulus, no detectable inflammation, and no structural damage to the nervous system or any other tissue. These syndromes likely result from abnormal pain amplification within the CNS (eg, more pain is felt than expected from any nociceptive input), start typically in adolescence or young adulthood, and manifest by pain experienced in different body regions at different times or simultaneously.
1) Somatic syndromes: Fibromyalgia, chronic headache, temporomandibular joint disorder, atypical facial pain, chronic back and neck pain
2) Visceral syndromes: Irritable bowel syndrome, bladder pain syndrome (formerly interstitial cystitis), chronic pelvic and abdominal pain, dysmenorrhea
3) Cognitive syndromes: Chronic fatigue syndrome, memory and attention disorder
4) Frequent comorbidities: Depression, anxiety, sleep disorder, PTSD, obsessive compulsive disorder, multiple chemical sensitivities/idiopathic environmental intolerances
Fibromyalgia
1. Epidemiology: Prevalence is from 2% to 4% of the general population; female-to-male ratio of 2:1, like other chronic pain conditions. Fibromyalgia can develop at any age, including in childhood.
2. According to the American College of Rheumatology revised in 2016, diagnostic criteria of fibromyalgia require that all of four conditions are met:
a. Generalized pain, defined as pain in at least four of five regions, is present.
b. Symptoms have been present at a similar level for at least 3 months.
c. Widespread pain index (WPI) ≥ 7 and symptom severity scale (SSS) score ≥ 5 OR WPI of four to six and SSS score ≥ 9.
d. A diagnosis of fibromyalgia is valid irrespective of other diagnoses. A diagnosis of fibromyalgia does not exclude the presence of other clinically important illnesses (Figure 5-1).
3. The physical examination (with exception of diffuse tenderness), laboratory tests, and imaging are normal and helpful to exclude other disorders and to locate the pathology of the pain. Establishing the clinical diagnosis can often result in decreased testing/referrals as well as patient relief.
4. Nonpharmacologic treatment
a. Education about the nature of this condition (eg, pain does not equal damage) and emphasizing an active role in one’s own care is critical. A suggested website for patients is https://fibroguide.med.umich.edu/.
b. Simple interventions such as stress reduction, improved sleep patterns, and increased activity and exercise should be reinforced.
c. Psychological factors like catastrophizing and fear of movement are treatable by CBT.
5. Pharmacologic treatment
a. Should always be used in conjunction with nonpharmacologic strategies.
b. Medications with strong evidence include tricyclic antidepressants (TCAs) (amitriptyline, cyclobenzaprine), gabapentinoids (pregabalin, gabapentin), serotonin norepinephrine reuptake inhibitors (SNRIs) (duloxetine, milnacipran), and γ-hydroxybutyrate.
c. Medications with less evidence include selective serotonin reuptake inhibitors (SSRIs) (eg, fluoxetine, paroxetine, sertraline), low-dose naltrexone, and cannabinoids.
d. Nonsteroidal anti-inflammatory drugs (NSAIDs) can be used as adjuncts for musculoskeletal pain.
e. The use of opioids is discouraged, as it can increase centralized pain (see section on Opioid-Induced Hyperalgesia).
f. Treatment should consider psychiatric comorbidities. Patients with anxiety and sleep disorder should be preferentially tried on gabapentinoids, while patients with depression might benefit more from SNRIs. All patients should be tried on TCAs.
6. Other therapies
a. There is limited evidence for trigger-point injections, chiropractic manipulation, tai chi, yoga, acupuncture, and myofascial release therapy.
b. Treating with local therapy, despite the central nature of the disease, decreases nociceptive input and might therefore have some benefit.
 Figure 5-1. A: Widespread Pain Index. Note the number of areas in which the patient has had pain over the last week. In how many areas has the patient had pain? Score will be between 0 and 19. B: Symptom Severity Score. Fatigue, waking unrefreshed, and cognitive symptoms. For each of these three symptoms, indicate the level of severity over the past week using the following scale: 0 = No problem; 1 = Slight or mild problems, generally mild or intermittent; 2 = Moderate, considerable problems, often present and/or at a moderate level; 3 = Severe: pervasive, continuous, life-disturbing problems. The Symptom Severity Score is the sum of the severity of the three symptoms (fatigue, waking unrefreshed, and cognitive symptoms) plus the sum of the number of the following symptoms occurring during the previous 6 months: headaches, pain or cramps in lower abdomen, and depression (0-3). The final score is between 0 and 12. (With permission from Clauw DJ. Fibromyalgia and related conditions. Mayo Clin Proc. 2015;90(5):680-692. doi:10.1016/j.mayocp.2015.03.014.) |
Somatic Symptom and Related Disorder
1. According to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), the category of somatic symptom and related disorders encompasses disorders that are marked by prominent somatic symptoms as well as substantial distress and/or psychosocial impairment. The category includes the following specific disorders:
a. Somatic symptom disorder (SSD)
b. Illness anxiety disorder
c. Conversion disorder (functional neurological symptom disorder)
d. Psychological factors affecting other medical conditions
e. Factitious disorder
2. SSD: A DSM-5 diagnosis of SSD requires each of the following criteria:
a. One or more somatic symptoms that cause distress or psychosocial impairment.
b. Excessive thoughts, feelings, or behaviors associated with the somatic symptoms, as demonstrated by one or more of the following:
1) Persistent thoughts about the seriousness of the symptoms.
2) Persistent, severe anxiety about the symptoms or one’s general health.
3) The time and energy devoted to the symptoms or health concerns is excessive.
c. Although the specific somatic symptoms may change, the disorder is persistent (usually more than 6 months).
d. Of note:
1) SSD is an umbrella term intended to describe most of the patients who previously held diagnoses such as somatization disorder, pain disorder, and hypochondriasis (all somatoform disorders in Diagnostic and Statistical Manual of Mental Disorders, 4th edition [DSM-IV]).
2) Diagnosis does not require that the somatic symptoms are medically unexplained. In other words, symptoms may or may not be associated with another medical condition.
3) DSM-IV diagnosis of somatization disorder requires a specific number of complaints from among four symptom groups. The SSD criteria no longer have such a requirement; however, somatic symptoms must be significantly distressing or disruptive to daily life.
4) DSM-IV pain disorder is now classified as SSD with predominant pain.
3. Treatment
a. Pharmacologic treatment of concurrent mental disorders (eg, depression) may help; however, the primary intervention is psychotherapy, particularly CBT.
b. Patients also benefit from having a supportive relationship with a primary care physician, who coordinates all their health care, offers symptomatic relief, sees them regularly, and protects them from unnecessary tests and procedures.
Complex Regional Pain Syndrome
1. CRPS is a clinical diagnosis, based on the 2010 Budapest Criteria (sensitivity 0.99, specificity 0.68), endorsed by the International Association for the Study of Pain and must meet all of the following criteria:
a. Continuing pain, which is disproportionate to any inciting event
b. Must report at least one symptom in three of the four following categories:
1) Sensory: Reports of hyperesthesia and/or allodynia (ie, a light tap on the wrist causing significant pain)
2) Vasomotor: Reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry
3) Sudomotor/edema: Reports of edema and/or sweating changes and/or sweating asymmetry in affected areas
4) Motor/trophic: Reports of decreased range of motion and/or motor dysfunction (weakness, tremor, or dystonia) and/or trophic changes (hair, nail, skin)
c. Must display at least one sign at time of evaluation in two or more of the following categories:
1) Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch, temperature sensation, deep somatic pressure, and/or joint movement)
2) Vasomotor: Evidence of temperature asymmetry (>1 °C) and/or skin color changes and/or asymmetry
3) Sudomotor/edema: Evidence of edema, sweating changes, and/or sweating asymmetry
4) Motor/trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
d. There is no other diagnosis that better explains the signs and symptoms presented by the patient during examination.
2. Of note:
a. An inciting event is not necessary to make the diagnosis.
b. Compared with previous diagnostic criteria, presence of physical signs (rather than symptoms alone) is required for diagnosis and increased specificity from 0.41 to 0.68.
c. Symptoms occur distally, affect the extremities, and do not correspond to a nerve or root territory. Typically, isolated joints and the head/face are not involved.
d. Spreading along the ipsilateral side to involve the other extremity is possible; however, rarely, bilateral extremities are involved.
3. Epidemiology
a. CRPS is three to four times more common in women.
b. CRPS onset can occur at any age; however, the peak age of onset is 40 years for both males and females.
4. Two types of CRPS exist: Nerve lesion absence (CRPS I) and presence (CRPS II)
a. Type I: No nerve lesion; synonyms: reflex sympathetic dystrophy, Sudeck atrophy, reflex neurovascular dystrophy, algoneurodystrophy
b. Type II: Nerve lesion present; synonym: causalgia
5. Clinical stages (not reliable because of large interindividual variability)
a. Stage I (acute, 0-3 months): Pain (burning, aching), sensory abnormalities, edema, fluctuation in skin temperature, sweating, muscle spasm/joint pain, and rapid hair growth
b. Stage II (dystrophic, 3-6 months): Symptom progression, increased pain/sensory dysfunction, motor/trophic changes, joint stiffness, and muscle weakness
c. Stage III (atrophic, >6 months): Limited range of motion secondary to increasing pain, increased trophic changes, muscle and tendon atrophy
6. Ancillary diagnostic testing (not required to make diagnosis)
a. Temperature differences of >1 °C, measuring of swelling with measure band or water bath, sweat testing.
b. Magnetic resonance imaging (MRI) is mostly helpful to exclude alternate diagnosis and can show bone marrow edema of affected limb (not specific).
c. Radiography to compare bone mineralization of the affected and unaffected extremity (on the same film) can show patchy areas of deossification (low sensitivity).
d. Three-phase bone scan is a sensitive (0.7) and relatively specific (>0.75) tool for upper extremity CRPS within the first 5 months after onset. Proposed region of interest localization is over the metacarpophalangeal (MCP) joint of the affected hand, and phase 3 is acquired 2 to 3 hours after tracer injection. A positive finding is increased periarticular tracer uptake of the MCP joints of the affected hand. Diagnostic value decreases beyond 5 months after CRPS onset.Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
