Chronic Pain



Chronic Pain


Robert D. Helme



CHRONIC PAIN


Background


Definitions



  • 1. Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage.


  • 2. Chronic pain is pain continuing after the time of normal healing or pain of any source present for more than 6 months.


  • 3. Other useful terms, especially in cancer pain:



    • a. Breakthrough pain is pain that occurs unexpectedly in the presence of stable background analgesia.


    • b. End-of-dose failure is pain that occurs between regular doses of analgesic due to decreasing effective tissue levels between doses.


    • c. Incident pain is pain on movement and implies a musculoskeletal origin or bony involvement by cancer.


    • d. Rebound pain is excessive pain that follows the cessation of analgesic effect.


Epidemiology



  • 1. Depending on the definition, up to 20% of adult patients seen by primary care physicians have chronic pain.


  • 2. Chronic pain increases with age from 20 to 60, mostly due to arthritic conditions. It then reaches a plateau before a decline in frequency occurs around age 80.


  • 3. About 50% of patients with cancer have pain at some stage of their disease and it often becomes the focus of clinical management.


The Biopsychosocial Model of Chronic Nonmalignant Pain



  • 1. The relationship between the amount of nociceptive stimulus and the degree of pain reported or pain-related behaviors depends on social, psychologic, and biologic factors.


  • 2. The level suffering and the affective and behavioral expression of the pain are mediated by characterological and cognitive reactions to the nociceptive stimulus and its environmental context (e.g., cancer pain engenders fear and exaggerates the experience of pain).


  • 3. Changes in the pain experienced, the mood of the patient, and the behaviors exhibited by the patient are often not synchronous. An improvement in pain is not always followed by a similar improvement in mood and function.


  • 4. Management of chronic pain requires that the treating physician incorporates the multidimensional nature of the pain experience, adjusts treatments, and advices accordingly.



Classification

Pain can be classified by its pathogenetic mechanism.



  • 1. Nociceptive pain: Caused by direct tissue injury with resultant stimulation of nociceptors on afferent Aδ and C fibers.



    • a. Examples of deep somatic nociceptive pain include arthropathy and back pain.


    • b. Superficial somatic nociceptive pain includes skin damage from trauma, chemical and thermal stimuli, and irritation of mucous membranes.


    • c. Visceral nociceptive pain can result from lesions in the capsules of solid organs or distention of a hollow viscus.


  • 2. Neuropathic pain: Caused by damage to sensory components of the nervous system and is independent of somatic damage.



    • a. Peripheral neuropathic pain is derived from activation of afferent nerves, especially those associated with nociceptors; examples include postsurgical injury, postherpetic neuralgia, diabetic neuropathy, traumatic neuroma, nerve root compression of irritation, phantom limb pain, the neuralgias, and complex regional pain syndrome type 2 (causalgia; CRPS-2).


    • b. Central neuropathic pain occurs when pathology of central neuraxis elements is involved in the transmission of nociceptive stimuli, for example, stroke, spinal cord trauma, syringomyelia, and multiple sclerosis that affect the thalamus, spinothalamic tract, or dorsal root entry zones.


  • 3. Psychologic pain: This is the most common type and is associated with psychologic factors (anxiety and depression) in response to a general medical disorder. Examples are found in Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV).


  • 4. Mixed: Examples include cancer and degenerative spine disease.


  • 5. Uncertain: Examples include fibromyalgia and complex regional pain syndrome type 1 (reflex sympathetic dystrophy; CRPS-1).


Pathophysiology


Physiologic Mechanisms



  • 1. Pain pathways



    • a. Nociceptors (e.g., ion gated-vanilloid, ligand gated-opioid, 5-hydroxy tryptamine [5HT]) are situated on small-diameter primary afferents (mechanical, thermal, chemical, and polymodal) that enter the dorsal horn of the spinal cord terminating predominantly in laminae 1, 2 (nociceptor-specific neurons) and 5 (wide dynamic range neurons).


    • b. Modified afferent information is transmitted to relay nuclei in the brainstem and medial and lateral thalamus predominantly via the spinothalamic pathways.


    • c. Thalamic impulses are transmitted to primary somatic cortex ([sensorimotor cortex] SM1, SM2), limbic cortex (cingulate and insula), and prefrontal cortex.


    • d. Descending modulation (excitatory and inhibitory) occurs via descending tracts originating in the periaqueductal gray matter and reticulospinal pathways (dorsolateral fasiculus in the spinal cord).


  • 2. Sensitization



    • a. Peripheral sensitization of nociceptors occurs from repeated or constant noxious and nonnoxious stimulation. Mechanisms include:



      • 1) Inflammatory mediators, cytokines, prostaglandins, neuromediators, and trophic factors


      • 2) Ephaptic transmission


      • 3) Sympathetic nervous system modulation


    • b. Central sensitization occurs through



      • 1) Upregulation of excitatory systems (e.g., glutamate via N-methyl D-aspartate [NMDA] receptors)



      • 2) Inhibition of inhibitory systems (e.g., GABA, glycine)


      • 3) Altered nervous system tissue or function (e.g., glial proliferation, neuronal dropout, sodium channel overexpression)


Neuropathic Pain Mechanisms



  • 1. Spontaneous and ectopic activity in damaged afferent mechanosensitive neurons.


  • 2. Ectopic activity in remaining C fibers after damage to other fiber types; this may be responsible for maintenance of central sensitization of neuropathic pain.


  • 3. Central sensitization



    • a. Windup: increased responsiveness of neurons to repetitive “C” fiber input with lowered response threshold, temporal summation, and spread of receptor fields


    • b. Deafferentation hypersensitivity


Visceral Pain Mechanisms



  • 1. High-threshold receptors that are normally active when there is acute injury become sensitized with prolonged stimulation.


  • 2. “Silent” mechanoreceptors that are quiescent normally become active to polymodal stimuli during visceral inflammation.


  • 3. The dorsal column transmits some visceral nociceptive information, together with other traditional nociceptive pathways.


  • 4. Visceral pain causes activation of a different part of the anterior cingulate cortex compared to somatic pain.


  • 5. With a lower density of innervation of an organ, there is less temporal and spatial resolution of visceral pain.


  • 6. Referred pain and autonomic responses have a lower threshold for being expressed when there is visceral pain.


Prognosis



  • 1. The patient’s quality of life with pain is determined by the broader context of physical activity, mood, and social function. Prognosis is good if these factors can be controlled.


  • 2. Chronic pain responds poorly to pharmacologic therapy.



    • a. About 30% of patients have a satisfactory long-term response to opioid therapy alone. Half, however, discontinue opioids because of toxicity or other reasons.


    • b. Up to 50% of patients with neuropathic pain have moderate pain reduction with non-narcotic adjuvant drugs (as listed further on, they include antiepileptic and antidepressant drugs). Only 10% to 20% of patients will have complete pain relief with this approach. The analgesic effect of these second-line drugs decreases with time.


  • 3. About 85% of patients with cancer pain will have a satisfactory response to conventional management with narcotic and non-narcotic medications. Factors that predict a poor response in cancer pain include neuropathic pain, incident pain (pain on movement), multiple pains from differing mechanisms, pain that has become persistent, adverse effects of treatment that are difficult to control, and a history of drug or alcohol abuse.


  • 4. In patients with chronic nonmalignant pain, maladaptive psychosocial factors have been termed “yellow flags” and include the following:



    • a. Maladaptive Attitudes and Beliefs



      • 1) Belief that pain implies ongoing damage or will be severely disabling.


      • 2) Belief that pain must be abolished before improvement in physical function is possible.


      • 3) Catastrophic misinterpretation of pain-related experiences.


      • 4) Belief that pain is uncontrollable.


      • 5) Belief that passive treatment (e.g., medications) is more helpful than active (participatory) treatment (e.g., rehabilitation).


    • b. Maladaptive Behaviors



      • 1) Use of extended rest to relieve pain.



      • 2) Reduced activity levels, particularly with personal activities of daily living (ADLs).


      • 3) Excessive reliance on aids.


      • 4) High intake of alcohol and other substances since the onset of pain.


      • 5) Irregular participation in physical exercise.


    • c. Poor Prior Diagnostic and Treatment Experiences



      • 1) Health care professional sanctioning of disability and inadequate provision of interventions that will improve function


      • 2) Conflicting diagnoses or advice concerning functional ability


      • 3) Health care professional focus on a biomedical perspective


      • 4) Failure to meet overoptimistic estimates of the benefits of treatments


    • d. Maladaptive Emotional Responses

      These include frustration, depression, anger at self and others, anxiety (including heightened sensitivity to benign bodily sensations, or hypervigi-lance), and fear of movement.


    • e. Dysfunctional Family Relationships



      • 1) Presence of an overprotective or solicitous spouse


      • 2) Poor general family relationships


      • 3) Lack of social support


    • f. Work Conditions



      • 1) Unsupportive management at the workplace


      • 2) Unhappy work environment


      • 3) Limited possibilities for a graduated return to work


      • 4) Lack of alternative work opportunities


Diagnosis


Diagnostic Formulation



  • 1. Should include a medical diagnosis (where possible), the psychologic (both affective and cognitive) and social factors that are modulating the pain experience, and the behaviors exhibited by the patient and the family.


  • 2. A central goal is to identify correctable pathologies if possible.


General Assessment



  • 1. Should also include an assessment of the goals and targets of the patient.


Medical Assessment



  • 1. Should include a thorough description of the pain complaint.


  • 2. The site of pain and its radiation and referral.


  • 3. The severity of the worst pain, least pain, and average pain should be scaled using a rating scale (e.g., The Brief Pain Inventory [BPI]):



    • a. Numeric rating scale (0-10, 0-20, or 0-100)


    • b. Verbal rating scale (e.g., mild, moderate, severe, horrible, excruciating)


    • c. Visual analog scale (VAS) (marking on a 10-cm line how severe the pain is with anchors of “no pain” and “most severe pain” on the ends or with progressive numerical markers; BPI, Gracely Box Scales)


  • 4. The temporal profile: continuous, intermittent, paroxysmal, or persistent pain.


  • 5. Factors modulating the intensity of pain, in particular precipitating, aggravating, and relieving factors.


  • 6. Quality descriptors. Useful examples taken from the McGill Pain Questionnaire include aching, sharp, burning, stabbing, and throbbing.


  • 7. Accompanying autonomic features including dystrophic skin, nail, and hair changes, and localized changes in skin temperature, sweating, and color should be noted.


  • 8. Other neurologic symptoms (dysesthesiae such as formication and electricity experiences, paresthesiae, analgesia) and muscular symptoms (weakness, stiffness, and joint restriction) should be noted.



  • 9. Certain features suggest serious underlying disease and warrant further evaluation: pain that wakes the patient at night; pain that is persistent and not modified by any analgesia; systemic features like unexplained weight loss, fever, or the patient complaining that they feel unwell; symptoms that suggest specific organ disease; and progressive neurologic deficit.


  • 10. Beyond a reasonable initial workup, the relentless pursuit of a “definitive” diagnosis is discouraged unless the above factors pertain.


Affective Presentation



  • 1. Ideally, this axis should be quantified, either by the means of standardized psychometric questionnaires or by the means of self-monitoring methods (numeric measures, diaries). However, it is possible to judge effect broadly from the clinical encounter and the impression should be recorded as an essential part of the pain history and examination.


  • 2. Anxiety can range from mild irritation to a defined psychiatric disorder with panic attacks (e.g., post-traumatic stress disorder). The Beck Anxiety Inventory is one good measure for quantifying anxiety symptoms. In anxiety states, there is frequently increased somatic awareness of benign symptoms and there is often misinterpretation (often exaggeration) of these symptoms.


  • 3. Depression varies from mild dysphoria to severe depression with suicidal ideation. Somatic symptoms of depression (insomnia, lack of energy, weight change) are frequently part of the chronic pain syndrome and should not be automatically attributed to depression. Suicidal ideation should be assessed in all patients with chronic pain. The Beck Depression Inventory, the Zung Depression Scale, and the Center for Epidemiological Studies-Depression Scale are useful measures. The Geriatric Depression Scale is more suitable for older people.


  • 4. Fear of movement has been identified as a strong affective factor predicting disability. The Tampa Kinesiophobia Scale is one measure to quantify this factor.


  • 5. Anger and hostility toward self, health professionals, relatives, and workplace management should be identified. Patients are also often frustrated by the lack of improvement in their condition.


Psychiatric Disorders as a Primary Explanation for Pain



  • 1. This diagnosis should be made with care. The prevalence of true, or primary, psychogenic pain is low. Preferably, this should be assessed by a psychiatrist or psychologist in the setting of a multidisciplinary clinic. Examples include somatoform disorders, conversion disorders, hypochondriasis, and psychogenic pain disorder (see DSM-IV for diagnostic details of these entities).


Behavior Assessment



  • 1. Health-seeking behaviors should be recorded and, if possible, quantified. For example, the number of times the patient has visited the local doctor in the previous week, the number of specialists that the patient has consulted or intends to consult, and the number of medications taken.


  • 2. Pain-specific behaviors such as wincing, guarding, and moaning are noted.


  • 3. Many patients are deconditioned with generalized weakness and stiffness. Activity-related behaviors such as avoidance of certain activities and extended rest periods should be evaluated. The ADLs and social activities in which the patient participates should be quantified.


  • 4. “Target behaviors.” The patient should be asked to identify realistic goals that can be accomplished in the course of treatment.


Cognitive Processes Relating to Pain



  • 1. Cognitive processes are important for modifying the pain experience. These attitudes, beliefs, or perceptions should be identified and corrected in the course
    of treatment. Relevant examples of psychometric tests include the Survey of Pain Attitudes and the Coping Strategies Questionnaire.


  • 2. Beliefs about pain include the following:



    • a. That it implies a serious or potentially terminal illness.


    • b. Patients who believe that they can control their pain have better moods, whereas patients who believe that their pain is not controllable or only controllable by medication or by their health care providers have poorer moods.


    • c. Patients who believe that they can achieve their goals despite their pain function better and have a more positive affect.


    • d. Beliefs about hurt, harming the body part, and creating further injury result in avoidance of use of the body part and worsen pain disability.


  • 3. Coping styles and strategies. Patients who by nature avoid facing problems do worse than those who confront life problems. Passive coping strategies and emotional reactivity lead to a worse prognosis.


Psychosocial Variables



  • 1. May be important in the management of chronic pain, including the following:



    • a. Relationships with significant others, in particular, the degree of solicitousness in the relationship


    • b. Work environment


    • c. Social supports


    • d. Home environment and immediate environs


Other Issues



  • 1. These include litigation and spiritual attitudes. The latter is particularly relevant in cancer pain management and in assessing the risk of suicide.


Physical Signs in the Examination of the Patient with Chronic Pain



  • 1. A thorough musculoskeletal and neurologic examination should be performed. The neurologist should observe deformity, joint passive and active range of movement, crepitus, and signs of inflammation, including end-of-range pain and local tenderness. As part of the musculoskeletal examination, the number of “fibrositis” tender points should be determined.


  • 2. Neurologic signs include



    • a. Diminished or absent sensibility to primary sensory modalities other than pain, including light touch, cold, warmth, vibration, and position sense and the correspondence to recognize anatomical distribution


    • b. Hypoalgesia (hypalgesia): Reduced sensation, categorized by anatomic distribution (e.g., dermatome, nerve).



      • 1) Hyperalgesia: Increased pain reported from a stimulus that is normally painful (mainly pinprick but includes mechanical, thermal, or chemical stimuli), including a lowered threshold to response. This phenomenon is often found in a nonanatomic distribution.


      • 2) Hyperpathia: Increased reaction to a painful stimulus (usually mechanical but may be thermal) especially to repetitive stimuli and often accompanied by an increased threshold to the noxious stimulus. Often found in a nonanatomic distribution. There may be persistence of the induced pain for seconds or up to minutes to hours.


      • 3) Allodynia: Pain due to a stimulus that does not normally provoke pain (e.g., touch, brushing the skin, warm and cool stimuli).


Special Pain Syndromes


Nociceptive Pain



  • 1. This is the pain arising from pain receptors on primary afferent nerves in bones, muscles, joints, connective tissues, and skin.



  • 2. It is described as dull or aching, with sharp momentary sensations superimposed, although many other descriptors are used by patients. The pain is well localized to the site of pathology and tenderness (mechanical pressure hyperalgesia) is felt frequently.


  • 3. There may be solely or additional referral of pain, which can mimic neuropathic-type pain. For example, disc disruption can produce sciatica, even without root compression. Sclerotogenous pain, having its origin in bone, periosteum, and tendons, can be referred to distant sites.


  • 4. Movement tends to exacerbate the pain.


  • 5. Signs of inflammation are variably present.


Neuropathic Pain

May 28, 2016 | Posted by in NEUROLOGY | Comments Off on Chronic Pain
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