1. Presented by
Dr. Subrat Kumar Nayak
2nd
Year Post Graduate Trainee
Moderator: Dr. Y. Arun Kumar Singh
Department of Anaesthesiology & Critical Care
Regional Institute of Medical Sciences, Imphal
2. What is PAIN?
• “An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage or described
in terms of such damage”
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3. Various Descriptors of Pain
Somatic pain caused by the activation of pain receptors in either the
cutaneous (the body surface) or deeper tissues (musculoskeletal tissues).
Visceral pain that is caused by activation of pain receptors from infiltration,
compression, extension or stretching of the thoracic, abdominal or pelvic
viscera (chest, stomach and pelvic areas).
Neuropathic pain caused by injury to the nervous system either as a result of
a tumor compressing nerves or the spinal cord, or cancer actually infiltrating
into the nerves or spinal cord.
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4. Acute pain: short-lasting and manifesting in objective ways that can
be easily described and observed. It may be clinically associated
with diaphoresis and tachycardia. It can last for several days,
increasing in intensity over time (subacute pain), or it can occur
intermittently (episodic or intermittent pain). Usually related to a
discreet event for onset: post op, post trauma, fracture, etc
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5. Chronic pain:
Long-term and typically defined if it lasts for > three months.
It is more subjective and not as easily clinically characterized as
acute pain and is more psychological.
This kind of pain usually affects a person's life, changing
personality, their ability to function, and their overall lifestyle.
Chronic pain has a psycho-social component that must be dealt
with the clinical picture before depression becomes a part of
multi-factorial disease.
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19. What is Chronic Pain?
Chronic pain is pain that:
– continues a month or more beyond the
usual recovery period for an injury or illness
or
– goes on for months or years due to a
chronic condition.
The pain may not be constant but disrupts daily
life.
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20. Dimensions of Chronic Pain
Loneliness Hostility
Social Factors
Anxiety Depression
Psychological Factors
Pathological Process
Physical Factors
TIME
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25. Neuralgia – an extremely painful condition consisting of recurrent
episodes of intense shooting or stabbing pain along the course of the
nerve.
Causalgia – recurrent episodes of severe burning pain.
Phantom limb pain – feelings of pain in a limb that is no longer there
and has no functioning nerves.
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29. COMPLEX REGIONAL PAIN
SYNDROMES(CRPS)
• Neuropathic pain that involves upper and lower extremities.
• Reflex sympathetic dystrophy and causalgia are replaced by
CRPS I , CRPS II.
• CRPS type I: follows minor trauma.
• Preceeding events are trauma, surgery, sprain, fracture,
dislocation.
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35. Fibromyalgia Syndrome
Etiology is unknown.
3 views of pathophysiology have emerged:
Central Nervous System (neurogenic)
generalized pain
increase in CSF substance P
decrease in serum and CSF serotonin
Muscle Pathology
– decreased oxygen tension and blood flow
– abnormal muscle biopsies
– weakness
Psychopathology
anxiety, depression
(Loesser et al, 2001; Portenoy et al, 1996; Wall et al, 1994)
36. Clinical Characteristics
Pain (musculoskeletal tenderness)
Lightheadedness, dizziness, syncope
Fatigue
Chronic insomnia; sleep disturbance
Cognitive deficits/short-term memory loss
Depression/anxiety
Numbness, dysesthesia in hands and feet
(Loeser et al, 2001)
37. Diagnosis
Based on the 1990 ACR
classification guidelines:
• 1 historical feature + 1 physical finding
• Historical feature = widespread (axial) pain of 3 months
or more
• Physical finding = pain in at least 3 of the 4 body
segments + a finding of at least 11 tender points on
digital palpation of 18 designated tender points
(Merskey et al, 1994; Portenoy et al, 1996; Wall et al, 1994; Wolk M, 2002)
39. POST HERPETIC
NEURALGIA(PHN)
Intractable pain that develops as a sequel of acute herpes zoster
infection (AHZ).
Pain from AHZ resolves usually within 3-4 weeks and if pain lasts
longer than 4-6wks PHN should be suspected.
In AHZ large myelinated fibers are destroyed whereas in PHN
pain processing by small fibers is compromised.
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40. Typically presents with unilateral pain in dermatomal
distribution.
Treatment:
Sympathetic blockade during attack
Antidepressants, anticonvulsants, opioids.
TENS.
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41. Trigeminal Neuralgia (TN)
TIC DOULOUREUX
classically presents as a painful, unilateral affliction of the face,
characterized by brief electric-shock-like pain, limited to the
distribution of one or more divisions of the trigeminal nerve.
Pain is commonly evoked by trivial stimuli, including washing,
shaving, smoking, talking and brushing the teeth, but may also
occur spontaneously. The pain is abrupt in onset and termination
may remit for varying periods.
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43. Diabetic neuropathy
Peripheral neuropathies may b present in 65% of IDDM patients.
Chronic sensorimotor distal polyneuropathy is the MC type.
Management:
Control of blood glucose and pharmacologic therapy.
Gabapentin and Pregabalin appear to be effective
TCAs are also effective but not SSRIs
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45. 5/1/2017 Chronic Pain Management 45
Phantom Pain
Occurs in as many as 80% of amputees.
Treatment includes use of opioids, gabapentin, NMDA
antagonist & antidepressants
51. Pain
Step 1
± Nonopioid
± Adjuvant
Pain persisting or increasing
Step 2
Opioid for mild to moderate pain
± Nonopioid ± Adjuvant
Pain persisting or increasing
Pain persisting or increasing
Step 3
Opioid for moderate to severe pain
± Nonopioid ±Adjuvant
Invasive treatments
Opioid Delivery
Quality of Life
Modified WHO Analgesic Ladder
Proposed 4th
Step
The WHO
Ladder
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52. PHARMACOLOGIC CONTROL
About half of hospitalized patients who have pain are
under-medicated.
Children are at particular risk of poor pain control
methods.
Medications are given as:
PRN : “as needed”
As a prescribed schedule
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57. ACCUPUNCTURE:
• Useful adjunct for patients with chronic musculoskeletal
disorders and headaches.
• Technique – insertion of needles in discrete anatomically
defined points called “MERIDIANS”.
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58. Transcutaneous electrical
nerve stimulation (TENS)
• Used widely in chronic pain
• All available trials used TENS as an adjuvant to
medication, and it’s possible the effects of TENS was
masked by the analgesic effect of medication
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59. Physical measures
Ice packs
Chiropractic/osteopathic manipulations
Massage
Yoga
Topical agents (Ben Gay/Icy Hot – with menthol, salcylates,
Capcaicin)
Local injections (steroids, lidocaine)
Glucosamine shown to help with osteoarthritis
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60. Psychological methods
Integral part of multidisciplinary approach to pain
management.
Self management techniques – cognitive methods,
relaxation, biofeedback.
Operant techniques.
Group therapy.
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61. Cognitive methods:
Based on assumptions that a patients attitude towards
pain can influence the perception of pain.
Maladaptive attitudes contribute to suffering and
disability.
Patient is taught skills for coping with pain either
individually or in group therapy.
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62. Biofeedback – provides biophysiological feedback to
patient about some bodily process the patient is unaware
of (e.g., forehead muscle tension).
Relaxation – systematic relaxation of the large muscle
groups.
Hypnosis – relaxation + suggestion + distraction + altering
the meaning of pain.
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63. OPERANT / BEHAVIOUR THERAPY:
• Based on premise that behaviour in patients with chronic
pain is determined by consequences of behaviour.
• Positive reinforcers aggravate the pain, negative
reinforcers reduce pain behaviour.
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65. Role of Invasive Procedures
Intractable pain*
Intractable side effects*
*Symptoms that persists despite carefully individualized
patient management
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66. SELECTION OF BLOCK:
Depends on
Location of pain
Its presumed mechanism
Skills of treating physician.
L.A ‘s can be applied locally, at peripheral nerve,
somatic plexus, sympathetic ganglia or nerve root,
centrally in neuraxis.
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73. SPINAL INJECTIONS:
Therapeutic effects of spinal injections are a combination
of primary physiologic changes that result from the
procedure and the secondary results arising from the
enhanced pain control that allow other treatments.
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74. Spinal cord stimulation
• Also called dorsal column stimulation.
• Produces analgesia by directly stimulating large A beta
fibers in dorsal columns of the spinal cord.
• Mechanism – activation of descending modulating
systems and inhibition of sympathetic outflow.
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75. Indications:
Sympathetically mediated pain
Spinal cord lesions
Phantom limb pain
Failed back surgery syndrome.
Technique: electrodes placed epidurally and connected to
an external generator.
Complications: infection, lead migration, lead breakage.
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76. Intracerebral stimulation
Deep brain stimulation may be used for intractable
cancer pain and rarely for intractable neuropathic pain of
nonmalignant origin.
Electrodes are implanted stereotactically into
periaqueductal and periventricular gray areas for
nociceptive pain.
Complications: intracranial hemorrhage and infection.
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77. Discography
Discogenic pain are non specific and
include non radicular back pain.
Pain worsens on sitting posture.
Functional discography involves
insertion of catheter and injecting LA.
Most feared complication is discitis
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81. Minimally invasive Lumbar Decompression
This minimally invasive procedure is
indicated in patients with low back pain &
neurogenic claudication associated with MRI
or CT evidence of central canal stenosis
secondary to facet hypertrophy.
It includes percutaneous laminotomy &
thinning of the ligamentum flavum to
increase the critical diameter of stenosed
spinal canal.5/1/2017 81Chronic Pain Management
82. Vertebroplasty &
Kyphoplasty
Indication: Vertebral compression fractures secondary to osteoporosis.
Technique: Vertebroplasty involves injection of Polymethylmethacrylate into
affected vertebral body. Kyphoplasty involves insertion of baloon before
injection of cement.
Complications: Pulmonary embolism, radiculopathy, spinal claudication &
paraplegia.
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83. Peripheral nerve stimulation
Indications:
treatment of neuropathic
pain ideally arising from
single nerve (occipital
neuralgia, supraorbital
neuralgia, peripheral
neuropathies)
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84. Intrathecal pumps
Option for individuals in
whom opioids are
medications at reasonable
doses or cause
unacceptable side effects.
Main indications are
patients with cancer pain
followed by pain of spinal
origin with failed back
spinal surgery.
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85. Novel Drug Therapies for
Treatment of Pain
Central Nociception:
Emerging Analgesic Targets
• Excitatory amino acid and NK receptors
• N-type Ca++
receptors
• N-acetylcholine receptors
• Adenosine (A1) receptors
• Cannabinoid (CB1) receptors
(Pappagallo M)
88. Preoperative considerations
Communicate with, and involve the patient in, perioperative management
decisions.
For opioids, continue baseline dose via appropriate route with
additional supplementation for the acute event carefully titrated to the pain
For antidepressants, continue low dose tricyclic antidepressants,
selective serotonin reuptake inhibitors, and selective noradrenaline
reuptake inhibitors; be aware of potential for serotonin syndrome
For anticonvulsants, continue perioperatively; if stopping, taper the dose
slowly to avoid withdrawal
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89. If patient has a spinal cord stimulator, turn this off perioperatively
If patient has an intrathecal drug delivery system, continue
perioperatively and supplement patient with additional analgesia for the
acute event enterally and/or parenterally; be aware of potentially serious
adverse effects of abrupt cessation of intrathecal medications
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90. Management of Chronic pain in
substance abuse disorder
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91. • Physical Dependence
– Abstinence syndrome induced by administration of an antagonist or
by dose reduction
– Usually unimportant if abstinence is avoided
– Assumed to exist after few days’ dosing but actually highly variable
– Does not independently cause addiction
• Addiction
– Disease with pharmacologic, genetic, psychosocial elements
– Fundamental features: loss of control, compulsive use, use despite
harm
– Diagnosed by observation of aberrant drug-related behavior
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92. Tolerance
Diminished drug effect from drug exposure
Varied types: associative vs. pharmacological
Tolerance to analgesia is seldom a problem in the clinical setting:
Tolerance rarely “drives” dose escalation
Tolerance does not cause addiction
Pseudoaddiction
Aberrant drug-related behaviors driven by uncontrolled pain
Reduced by improved pain control
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93. The prevalence of opioid abuse in chronic pain patients ranges between
20-24% across health-care settings.
Further, it has been reported that 3.3% to 11.5% of chronic pain patients
with a history of SUD may develop opioid addiction or abuse, whereas only
0.19% to 0.59% of those without a prior or current history of SUD develop
the same.
Opioid-induced hyperalgesia is seen in Substance Use Disorder (SUD
patients)
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97. REFERENCES
Miller’s Anaesthesia, 8th
edn.
Barash’s Clinical Anaesthesia, 7th
edn.
Raj PP: Practical Management Of Pain .
Wall PD, Melzack OC: Text book of pain.
ISA Journal On pain.
Gowri devi M; Chronic pain Management-Psychological aspects in current concepts
in pain management.CME abstract 1998.
The Journal of Neuroscience, February 2007, 27(9): 2357-68.
www.who.int/icd11
Addiction Science & Clinical Practice 2013; 8:21
5/1/2017 97Chronic Pain Management
Colored portrait picture of a white woman, shoulder length brown hair with a worried look on her face . She is on the right side of the page.
Episodes of neuralgia occur suddenly and without apparent cause. Someone with causalgia may report that it feels like my arm is pressed against a hot stove. Typically follows a traumatic injury like a gun shot wound or stabbing and occurs at the site of injury. Is experienced well after the wound has healed.
Phantom limb pain – example might be burning sensation in your toes after the limb and foot has been amputated. Person can experience a sense of their limb moving. Can persist for months and years. Pain can be felt as shooting, burning, or cramping (e.g., feel like hand is clenched with finger nails digging into the hand).
Fibromyalgia syndrome is not a subtype or form of arthritis. Although it is associated with widespread pain, joint swelling and inflammation are not obvious. The soft tissues that are painful in this syndrome appear to be the ligaments, muscles, bursae, tendons, and fascia. In 1990, the American College of Rheumatology established criteria for the diagnosis of fibromyalgia syndrome, including a history of widespread musculoskeletal pain of more than 3-months’ duration and pain upon palpation of specific tender points (11 of 18, with 9 bilateral). The locations of the tender points include the occiput, cervical spine, trapezius, supraspinatus, second rib, lateral epicondyle extensor muscle, gluteal region, greater trochanter, and knees (all bilateral). In view of the tenderness in these areas at stimuli not normally painful, some have viewed fibromyalgia syndrome as a disorder of “widespread allodynia.”
Fibromyalgia syndrome has been reported in all age groups and in many ethnic groups. In adults, the syndrome is 4 to 7 times more common in women than in men. The highest prevalence is in women between 50 and 60 years old. Even though the syndrome may occur in association with other disorders such as systemic lupus erythematosus or rheumatoid arthritis, its presentation is not a “transition” to one of these or other disorders.
Loeser JDF, Butler SH, Chapman CR, et al. Bonica’s Management of Pain. 3rd ed. Baltimore: Lippincott Williams Wilkins; 2001:581.
Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:145-151.
Wall PD, Melzack R. Textbook of Pain. 3rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:579-580.
It has been suggested that the typical patient with fibromyalgia syndrome is a middle-aged woman who complains to her doctor that “everything hurts.” In evaluating a patient, care must be taken to distinguish between a myofascial syndrome trigger point and a tender point (which occurs in fibromyalgia). Although some individuals with fibromyalgia syndrome may have an occasional trigger point upon examination, the two disorders are not synonymous.
Other symptoms associated with fibromyalgia are throbbing occipital pain of muscle contraction headache, prolonged morning stiffness, chest wall pain, breast area pain, low back pain or sciatica-like radiation of pain, bursitis, tendonitis, irritable bowel, diarrhea, constipation, frequency/urgency.
Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3rd ed. Baltimore: Lippincott Williams Wilkins; 2001:550.
The 1990 guidelines for a diagnosis of fibromyalgia are the most widely used criteria. A diagnosis consists of one historical feature and one physical finding.
The historical feature is widespread pain of 3 months or more. Pain is considered widespread when all of the following are present: pain in the left and the right sides of the body, pain above and below the waist. Additionally, axial skeletal pain must be present (cervical spine or anterior chest or thoracic spine or low back). In this definition, shoulder and buttock pain is considered as pain for each side.
The physical feature is pain in 11 of 18 tender point sites on digital palpation. The 18 tender points are: occiput, low cervical, trapezius, suprespinatus, second rib, lateral epicondyle, gluteal, greater trochanter, knees. Digital palpation should be done with an approximate force of 4 kg. For a tender point to be considered “positive,” the patient must state that the touch was painful, not just tender. The presence of a second clinical disorder does not rule out the diagnosis of fibromyalgia.
Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed. Seattle, WA: IASP Press; 1994:46.
Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:146.
Wall PD, Melzack R. Textbook of Pain. 3rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:580.
Wolk, M. The diagnosis and treatment of fibromyalgia. http://www.systoc.com/CMEcourses/wolk (accessed 5/23/02)
Generally the treatment of fibromyalgia sydrome (FMS) is unsatisfactory, yet there are many therapeutic options that can lessen the degree of pain, improve functionality and help patients cope with the disorder.
Often a great deal of relief is provided simply by explaining the nature of the syndrome and reducing the patient’s anxiety by ruling out a more serious, life-threatening condition—assuring the patient that FMS will not cause crippling or reduced life expectancy.
The first, and possibly most important, step in treatment is patient education and support, both by the physician and medical staff, as well as a FMS support group, if possible.
Equally important for the FMS patient is exercise, as deconditioned muscles are more prone to microtrauma, and inactivity leads to dysfunctional behavioral traits. All FMS patients need to have an ongoing home exercise program with muscle stretching, gentle strengthening and aerobic conditioning. It is important to remember that exercise for the FMS patient is health training, not sports training; should be non-impact exercise; should be done for a total of 30 minutes each day (10-minute or 15-minute sessions are fine); and strength training should be concentric and avoid eccentric muscle contractions.
Pharmacologic treatments have been used with varying degrees of success in FMS patients, the most effective drugs being tricyclic antidepressants and analgesics.
Poor pain control is based on misperceptions of pain controlling medications – e.g., fear of addiction. Children, for fear of needles or lack of knowledge about pain-killer medications, may request medications less.
Capsaicin (Zostrix) – red hot chili pepper juice – used for centuries in S. America, burns for first few days then wears out substance P in pain receptors
PT/chirpracter/massage/yoga/acupuncture in some studies equally effective in certain conditions like low back pain
NSAIDs – beware of GI side effects and platelet effects, though the Salcylate class and Diflunisal have less of these effects. NSAIDs in studies shown to decrease narcotic use by up to 40% in things like wide-spread boney mets
Relaxants – soma, flexeril, benzodiazepines
Biofeedback for the treatment of chronic pain appears to be no more effective than relaxation methods. Relaxation may work in two ways: 1) reducing muscle tension; and 2) helping the patient better manage stress and anxiety. Relaxation exercises are frequently used in preparing a pregnant women for the delivery of her child. Relaxation may also stimulate the release of endogenous opioids, as well as boosting immune function. Evidence suggests that its effects are modest but useful in combination with other methods.
Mechanism by which hypnosis works for some pain conditions, particularly acute pain such as that during surgery, is not well understood. Cognitive methods of pain control appear to be as effectives as hypnosis.
Research is targeted at the isolation of novel compounds that will produce profound central antinociceptive effects by acting on the following receptors:
Excitatory amino acids (EAAs) glutamate and aspartate, as well as several neuropeptides—such as substance P, calcitonin gene-related peptide, cholecystokinin, and neurokinin—are the neurotransmitters of nociception found on the C-fibers entering the dorsal horn of the spinal cord. By acting on several receptors such as N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, kainate, the metabotropic receptors, and the neurokinin receptors, these neurotransmitters can induce central sensitization.
Blockade of the N-type (neuron-specific) calcium channels within the dorsal horn represents an alternative for intrathecal analgesia with opioids or local anesthetics. An N-type calcium channel blocker (ziconotide) derived from the venom of a predatory marine snail soon may be available for clinical use.
The activation of CNS adenosine A1 receptors also is pertinent to pain control, as demonstrated by intrathecal administration of adenosine in animal models.
Similarly, recent studies evaluated the role of cannabinoids, not only as antiallodynic and antihyperalgesic agents, but also as potentiators of opioid analgesia.
Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59.LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management.Cancer Pract. 2002;10(suppl 1):S14-S20 .
Some membrane components, recently identified and anticipated to be relevant to the various pathogeneses of pathologic pain and targets for analgesic drugs discovery, are the sensory neuron specific tetrodotoxin-resistant (TTX-R) voltage-gated sodium channels, opioid receptors, the vanilloid receptors (VRs), and the serotonin receptors.
In the DRG, 2 types of TTX-R voltage-gated sodium channels have been identified: the PN3 and NAN. After peripheral-nerve or tissue injury, the abnormal processing of pain may be contributed to alterations in the sodium channel expression and function.
The activation threshold of nociceptors also may be lowered by a direct modulation of heat or by mechanotransducer receptor proteins. The VR-1 receptor, for example, contributes to heat detection. Others among the emerging peripheral nociception channel and receptor targets include the following:
The alpha-2 adrenergic receptors—For example, the topical application of an alpha-2 adrenergic agonist causes local inhibition of noradrenaline release by acting on the adrenergic alpha-2 autoreceptors of the sympathetic endings.
The proton-sensitive channels—The H+-gated channel that is cloned is the acid-sensing ionic channel (ASIC), which is a member of the amiloride-sensitive/degenerin family and is expressed in some brain neurons, as well as in nociceptive neurons. The ASIC is transiently activated by rapid extracellular acidification (below pH 6.5) and desensitizes within a few seconds.
The nerve growth factor (NGF) receptor—An example is the tyrosine kinase (TrKA) receptor for NGF. The TrKA-NGF complex is internalized and retrogradely transported to the DRG cell body, where it initiates gene transcription that promotes upregulation of channels involved in pain transmission.
The N- or T-type current calcium channels—Following axonal injury, altered Ca++ signaling may contribute to hyperexcitability leading to neuropathic pain.
The purine receptors—Purinoceptors on sensory nerve terminals may be acted upon by ATP released from different cell types, thereby contributing to the initiation of pain.
Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59.