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Ragas dental college facical pain non odontogenic causes
1. FACIAL PAIN-NON ODONTOGENIC CAUSES
Dr. A.V. Srinivasan
MD.,DM.,Ph.D .,
D.Sc (HON).F.I.A.N.,F.A.AN.
Emeritus professor of Tamilnadu
Dr. M.G.R Medical University.
Adjunct Professor –IIT, Chennai
Former Head, Institute of Neurology-
Madras medical college.
Ragas Dental college 07-08-2011
2.
3. Chronic Pain
Understanding, Impact and
Awareness
We learn by thinking and the quality of the learning outcome
is determined by the quality of our thoughts
R.B. Schmeck
4. “Pain May be Inevitable, but Misery is Optional”
Dee Malchow
Pain constitutes nearly 40% of the total of patient visits to doctors. 1
“ByNature All Men/W en are alike but
om
byEducation widelydifferent”
1 Mäntyselkä et al. Pain as a reason to visit the doctor: a study in Finnish primary health care. Pain. 2001 Jan;89(2-3):175-80.
- Chinese
5. In 2001, Barry Furrow wrote “Pain is undertreated” in the American health-care
system at all levels.2
The term "opiophobia" has been coined to describe this remarkable clinical
aversion to the proper use of opioids to control pain.
The possible reasons for health-care providers' failures to properly manage pain
are many;
Occasional lack of knowledge about appropriate treatment choices for pain
management
A reflection of a Culture hostile to drug use
Threats of legal action.
Worry about tolerance and addiction and other adverse drug effects
Something as trivial as the lack of insurance cover, can lead to patients
suffering unnecessary pain as a result.
2. R.M. Marks and E.J. Sachar, "Undertreatment of Medical Inpatients with Narcotic Analgesics,"Annals of Internal Medicine, 78 (1973): 173.
6. Despite an essentially stoic and less demanding Indian patient; the
obligation to manage pain comes to the fore not only to complete the
perfection of a clinicians management.
But also, it is an independent entity with physical and psychological
components that in adherence to best practices can neither be ignored
nor treated such that adverse effects eclipse the malady.
This importance of pain management is further increased when
benefits for the patient are realized,
Early mobilization which tends to prevent the more dangerous
complication of a deep vein thrombosis;
Shortening hospital stay
Reducing costs
7. In late 2000, US Congress passed into law a
provision, which the president signed , that
declared the 10 year period beginning Jan 1 st
2001, as the Decade of Pain Control and
Research.
The American Pain Society has actively suppor ted
the Decade of Pain Control Research, and it has
been a focal point for the development of
numerous programs to advance awareness and
treatment of pain and funding for research.
8. • Pain is always a subjective experience
• Everyone learns the meaning of “pain” through experiences usually
related to injuries in early life
• As an unpleasant sensation it becomes an emotional experience
• Pain is a significant stress physically, emotionally
The International Association for the
Safety of Pain (IASP) defines pain an
unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described
in terms of such damage, or both.
(American Society of Anesthesiologists, 2002; Loeser et al, 2001; Merskey H et al, 1994; Portenoy et al, 1996)
9. Organic vs. psychogenic
Acute vs. chronic
Malignant or benign
Continuous or episodic
Perceiving Pain
• Algogenic substances – chemicals released at the site of the
injury
• Nociceptors – afferent neurons that carry pain messages
• Referred pain – pain that is perceived as if it were coming from
somewhere else in the body
10. ACUTE CHRONIC
Function To warn None (destructive)
Etiology Usually Clear Complex/obscure
Pt. Mood Anxiety/fear Depression/anger
MD impact Comforting Frustrating/draining
Role of Rx Control/cure Improve function/QOL
11. Types of Pain
Types of Pain
(Psychogenic)
(Psychogenic)
Pain arising from
Pain arising from Pain arising from
Pain arising from
pain receptors
pain receptors Pain with NO apparent cause
Pain with NO apparent cause
Nervous system
Nervous system
[Nociceptive Pain]
[Nociceptive Pain] (e.g. Low back pain or some
(e.g. Low back pain or some [Neuropathic Pain]
[Neuropathic Pain]
pelvic pain in women)
pelvic pain in women)
Peripheral
Peripheral
Central
Central
Superficical / /Somatic
Superficical Somatic Deep / /Visceral
Deep Visceral
(Brain and Spinal cord)
(Peripheral nervous
(Peripheral nervous
(Brain and Spinal cord) system)
system)
Keay, KA; Clement, CI; Bandler, R (2000). "The neuroanatomy of cardiac nociceptive pathways". in Horst, GJT. The nervous system and the heart.
Totowa, New Jersey: Humana Press. p. 304
13. IASP (International Association for the Study of Pain) expert multi-axial classification of chronic pain
Axis I: Anatomical location
Axis II: Systems
Axis III: Temporal Characteristics (intermittent, constant, etc.)
Axis IV: Patient’s Statement of Duration/ Intensity / severity
Axis V: Etiology
Example:
Mild post-herpetic neuralgia of T5 or T 6; 6 months ’ duration =
303.22e
Axis I: Thoracic region
Axis II: Ner vous system (central, peripheral, or autonomic); physical
disturbance/dysfunction
Axis III: Continuous or nearly continuous, fluctuating severity
Axis IV: Mild severity of 1 to 6 months
Axis V: Trauma, operation, burns, infective, parasitic (one of these)
(Loeser et al, 2001; Merskey et al, 1994)
14. Chronic pain has a
Hostility
Depression
psycho-social component
that must be dealt with
Psychological Factors before depression
Pathological Process
becomes a part of the
Loneliness
Physical Factors
Social Factors
clinical picture. Chronic
Anxiety
pain should be recognized
as a multi-factorial disease
state requiring intervention
at many levels.
A.G. Lipman, Cancer Nursing, 2:39, 1980 TIME
15. Chronic pain has high co-morbidity
Depression
Anxiety disorders
Sleep disorders
All diminish function and quality of life
Addressing these issues is essential to optimal pain
management
Give us the GRACE to acce pt with se re nity the thing s that canno t be chang e d the COURAGE to
chang e the thing s that sho uld be chang e d and the W ISDOM to kno w the diffe re nce
16. Chronic pain is NOT a normal part of aging.
Emotions play a key role in painful experience
Pain sounds a warning, signaling damage to tissues, and has survival value so pain receptors do not
adapt to prolonged stimulation and pain sensation may intensify as pain thresholds are lowered by
continued stimulation.
The 19th Century viewed pain as a solely physiological entity with two theories dominating – the
“specificity” & the “summation” theories. 8
Paradigm Shift:
Pain perception impulses are modified by ascending and by descending pain-suppressing
systems activated by various environmental and psychological factors.
1965 Melzack & Wall: Gate Theory of Pain marked a turning point in understanding transmission
and modulation of nociceptive signals, and recognition of pain as a psychophysiological
phenomenon.
The concept of Neuroplasticity was recognized and accepted adding dynamism to neuronal & brain
structure with neuroimaging of the central nervous system in three domains; anatomical, functional,
and chemical imaging helping measure changes in chronic pain.
Taken together these three domains have changed our thinking on pain; now considered an altered
brain state in which there may be altered functional connections or systems and components of
degenerative aspects of the CNS. 9
8) 11. J.A. Paice, C. Toy, and S. Short, "Barriers to Cancer Pain Relief: Fear of Tolerance and Addiction," Journal of Pain and Symptom Management, 16 July 1998): 1-9.
9) Quick Reference Guide for Clinicians No. 1a. AHCPR Publication No. 92-0019: February 1993
17.
18. Trauma/ injury initiates immediate
nerve impulses to brain
Injury to cells result in chemical
release
H+
K+
Substance P
Bradykinin
5HT
Phospholipids ⇒Prostaglandins
Blood vessels leak resulting in
inflammation
Stimulate C-fibres (slow response)
21. Αδ ( A delta)
Myelinated
Fast conductors
Gentle pressure and pain
Αβ (A beta)
Thinner – but still
myelinated
Fast conductors
Heavy pressure &temp
C - very thin
Slow conductors
PAIN, Pressure, temp &
chemicals
22. In chronic pain, the nervous system remodels
continuously in response to repeated pain signals
ner ves become hypersensitive to pain
ner ves become resistant to anti-nociceptive
system
If untreated, pain signals will continue even after
injury resolves
Chronic pain signals become embedded in the
central nervous system
(Marcus, 2000)
23. Pain-Sensing System in the
Malfunction in Chronic Pain
Acute pain:
Pain Pain-sensing signals are
initiated in response to a
Sensing stimulus
• They elicit a pain-
In chronic pain, relieving response
pain signals are
generated without
physiologic Chronic pain:
significance
Pain signals are generated
for no reason and may be
intensified
• Pain-relieving
mechanisms may be
defective or deactivated
(Illustration: Seward Hung, 2000)
24. Reticulospinal fibers from raphe nuclei project to dorsal horn of spinal cord and
release serotonin which stimulates interneurons to release enkephalin
Enkephalin inhibits transmission of pain and temperature signals in second
order neurons
Reticulospinal fibers from locus coruleus also project to dorsal horn of spinal
cord and release norepinephrine which inhibits pain and temperature signals by
an unknown mechanism
Mental illnesses such as depression decrease serotonin and norepinephrine
and lower pain thresholds while antidepressant drugs and therapies (e.g.,
exercise) which increase serotonin and norepinephrine levels raise pain
thresholds
25. Inferred from characteristics, etiology or pathophysiology
Types
Nociceptive
Neuropathic
Idiopathic
Therapeutic implications
(Portenoy et al, 1996)
26. Presumably results from ongoing activation of primary
afferent neurons responding to noxious stimuli
Pain consistent with degree of tissue injury
Described as aching, squeezing, stabbing, throbbing
Subtypes:
Somatic: related to activation of somatic af ferent
neurons
Visceral: related to activation of visceral af ferent
neurons
(Loeser et al, 2001; Portenoy et al, 1996)
27. Initiated by a primary lesion in the nervous system; believed to be
sustained by aberrant somatosensory processing in the peripheral or
central nervous system
Independent of obvious ongoing nociceptive activation
Burning, shooting, electrical quality; may be aching, throbbing, sharp
Subtypes:
Presumed “central generator”
deaf ferentation pain (central pain, phantom pain)
Sympathetically -maintained pain
Presumed “peripheral generator”
Polyneuropathies and mononeuropathies
(Portenoy et al, 1996)
28. Idiopathic Pain
Usually exists in the absence of an identifiable physical or
psychologic pathology that could account for pain
Uncommon in patients with progressive illness
Psychogenic Pain
Presents positive evidence of a predominant psychologic
contribution and may be labeled with a specific psychiatric
diagnosis
(Loeser et al, 2001; Merskey et al, 1994; Portenoy et al, 1996)
29. Greater understanding of the pathophysiology underlying chronic
pain syndromes
Scientific breakthroughs in molecular biology; insight into pain at
the molecular level
Advances in drug therapy (drug delivery technologies)
Multimodal therapy
Multidisciplinary teams, shared decision-making that includes
patients
Patients’ rights movement
(JCAHO, 1999; Loeser et al, 2001)
30. Progress in Chronic Pain Management:
Therapeutic Modalities for
Chronic Pain Management
Assessment
31. “Describing pain only in terms of its
intensity is like describing music only in
terms of its loudness”
von Baeyer CL; Pain Research and Management 11(3) 2006; p.157-162
32. Characterize the pain
Characterize the disease, relationship between
pain and disease and potentially treatable
etiologies
Clarify syndromes and infer pathophysiology
Determine need for urgent therapy
Identify other needs
Develop a therapeutic strategy
(Portenoy et al, 1997)
33. Components
History: temporal features, intensity, topography, quality,
exacerbating/alleviating factors
Physical Exam: determine existence of underlying pathology
Lab and Radiographic Tests: appropriate to pain syndrome
Assessment Tools
Pain Intensity Scales: VAS, NAS, “faces” scale
Multidimensional Pain Measures: Brief Pain Inventory, McGill
Pain Questionnaire
(Portenoy et al, 1997)
34. • Visual Analogue Scale (VAS)
No pain ----------------------------------- Worst pain
• Numerical Rating Scale
0 ------------------------------------- 10
Worst pain
No pain
imaginable
• Categorical Scale
None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10)
• Pain Faces Scale
0 2 4 6 8 10
No Hurts just a Hurts a little Hurts even Hurts a whole Hurts as much
hurt little bit bit more more lot as you can
imagine
• Brief Pain Inventory Shade areas of worst pain. Put an X on area that hurts most
(Cleeland, 1991; Jacox et al, 1994)
35. Progress in Chronic Pain Management
Therapeutic Modalities for Chronic
Pain Management
Treatment
37. Best evidence: TCAs
Inhibit both NA and 5-HT reuptake
TCAs are superior to SSRIs in pain management
TCAs are superior to the anticonvulsant
There is no consensus regarding which of the many TCA
derivatives is most effective.
The choice of TCA is therefore dictated largely by adverse
effects
Neurologic Complications of Cancer Therapy Current Treatment Options in Neurology 1999, 1.428-437
Litsedge, A Double-Blind Comparison of Dothiepin and Amitriptyline for the Treatment of Depression with Anxiety, Psychopharmacologia (Berl.) 19, 153--162 (1971)
38.
39. Major reason for seeking medical care.
90% is vasculr headache.
10% is mixture of inflammation,traction or
dilatation of pain sensitive structure.
A true commitment is a heart felt promise to yourself from which you will not
back down
- D. Mcnally
40. Pain
Referred pain
Pattern of referred pain
Success in life is a matter not so much of talent and opportunity
as of concentration and perseverance
- C.W. Wendte
41. History
Hx of present illness
Past medical hx
Family hx
Social hx
Physical examination
We possess by nature the factors out of which personality can be made, and to
organize them into effective personal life is every man’s primary responsibility
- Harry Emerson Fosdick
42. Clinical features suggesting serious cause
Crescendo
Early morning
Vomiting
Fever
Seizures & other neurological symptomes
Worst headache in my life
Known malignancy
Tenderness
43. Typical Neuralgias
1) Trigeminal neuralgia
• Characterized by recurring paroxysmal
severe pain, brief duration (seconds) in the
territor y of the trigeminal ner ve,
spontaneously or initiated by chewing,
talking, touching the af fected side of the
face.
• Unknown aetiology, an ar terial loop pushing
on the sensor y root in the posterior fossa.
• Females af fected more than males
• Analgesics, surger y, destruction of the
sensor y neuron, division of ner ve root.
44. Typical Neuralgias
2) Glossophar yngeal neuralgia
• Unknown cause
• Equal both sexes
• Severe, sudden episodes of pain in
the tonsil region one side only,
ipsilateral ear.
• Pain - severe for 1-2 hours, recur
daily
• Treated like trigeminal
45. Typical Neuralgias
3) Sluder’s neuralgia and Vidian
neuralgia
• Intractable pain in the nose, eye,
cheek and lower jaw.
• Could be due to lesion of the
sphenopalatine ganglion, or vidian
ner ve.
• Analgesics, vidian neurectomy
46. Posttraumatic neuralgia
Neuroma
Parietal & occipital
90% recover y
Experience can be defined as
yesterday’s answer to today’s problems
47. Atypical facial pain
Pain felt over the cheek, nose, upper
lip or lower jaw
Usually bilaterally symmetrical
Aching, shooting, burning,
accompanied by reddening of the skin
and lacrimation or watering of the nose
Lasts for hours, days or weeks
Psychological consultation, analgesics
48. Intracranial lesions
1) Central lesions
• Tumours of the brain stem, M.S.,
thrombotic lesions, metastasis, occult
naso-phar yngeal ca.
• No precipitant, sensor y loss.
2) Post herpetic neuralgia
• Herpes zoster may af fect trigeminal
ner ve ganglion
• Vesicular rash covers one division
commonly the 1 st with severe pain.
50. Headache is one of the commonest
symptoms in medical practice.
Aetiology:
1) Raised intracranial pressure
Due to tumours, abscesses, subdural
haematoma, brain haemorrhage.
2) Inflammation of the brain and
meninges
e.g. meningitis, cerebritis, others
51. 3) Migraine
Congenital predisposition
Triggered by hunger, cer tain foods, sleep -
too much or too little, hormonal variations,
stress.
Pathology-vascular dilatation
Females af fected more than males
? Proceeded by aura usually visual,
paraesthesiae of hands, weakness
Headache is unilateral or bilateral, af fects
any area of the head, aching or throbbing
of ten accompanied by nausea and
vomiting
Diagnosis - by histor y alone
Treatment - prevention by avoiding
precipitating factors, appropriate
medication.
52. 4) Tension headache
More common in adult females
Positive family histor y (40%)
Maybe associated with migraine
Produced by persistent contraction of
the muscles of the neck, head and face
Caused by emotional tension,
secondar y to other headaches, posture
habit
Treated by analgesics, muscle
relaxants, physiotherapy
53. 5) Cluster headache
90% are men
Age 20 - 30
Attacks occur in groups, no aura
Caused by vascular dilatation of
branches of external carotid
Triggered by histamines, alcohol
Treated by analgesics, anti-histamine,
steroids
54. Pain from temporalis muscles
Can arise from grinding teeth at
night (bruxism), impacted wisdom
teeth, temporomandibular joint
dysfunction, anxiety when the
patient clenches the jaws too tightly
Treatment: Refer to interested
dental surgeon .
55. Pain from upper neck muscles
Can radiate over the head
Treatment by physio-therapist or
rheumatologist
Pain from frontalis muscles
Usually due to bad posture at work
or while driving
Treatment: physio-therapy
56. Cer vical spondylosis
Pain mediates upwards from the neck to
the occiput or ver tex to the front of the
head, down to the shoulders
Due to cer vical discs prolapse
Diagnosis - x-ray
Treatment: Physio-therapy, referral to
rheumatologist
57. Temporal ar teritis
Due to acute inflammation of the ar ter y,
the cause unknown, af fects men and
women over the age of 60
Pain over the temples and frontal region,
intense, throbbing, tenderness over the
scalp, swelling and redness of the
overlying skin with general malaise, par tial
or complete loss of vision.
ESR Elevated
Treatment: Cor tisone, analgesics
58. Psychologic headache
Usually accompanied by
depression, anxiety
No organic lesion
It is a great misfortune not to possess sufficient wit to speak well
nor sufficient judgment to keep silent
La Broyers character
61. READ not to contradict or confute
Nor to Believe and Take for Granted
but TO WEIGH AND CONSIDER
My sincere thanks to P.Sampath
Hinweis der Redaktion
08/14/12 09:33 AM
08/14/12 09:33 AM Numerous surveys from the United States and Europe during the last decade have shown that 30% to 50% of adult patients in active therapy for a solid tumor experienced chronic pain. With advanced disease, the prevalence of pain increased to 90%. A recent survey by the IASP concluded that the inferred mechanism of pain is neuropathic in 40% of cases. In a very large survey of institutionalized elderly patients with cancer, the prevalence of pain was 27.4%, and pain was associated independently with age, gender, race, marital status, functionality, and cognitive status. Cancer pain is often associated with psychological distress and functional impairment. Unrelieved pain may significantly impaired quality of life . In the AIDS population, the prevalence rates range from 25% to 80%. This broad range reflects differences in populations studied and pain assessment methodologies. Bernabei R, Gambassi G, Lapane K, et al: Management of pain in elderly patients with cancer. JAMA. 1998;279:1877-1882. Caraceni A, Portenoy RK, a working group of the IASP Task Force on Cancer Pain. An international survey of cancer pain characteristics and syndromes. Pain . 1999;82:263-274. Cleeland CS, Gonin R, Harfield AK, et al: Pain and its treatment in outpatients with metastatic cancer. N Engl J Med. 1994;330:592-596. Heim HM, Oei TP: Comparison of prostate cancer patients with and without pain. Pain. 1993; 53:159-162. Portenoy, RK: Cancer pain. Pathophysiology and syndromes. Lancet. 1992; 339:1026-1031. Portenoy RK, Kornblith AB, Wong G, et al: Pain in ovarian cancer. Prevalence, characteristics, and associated symptoms. Cancer . 1994;74:907-915. Serlin RC, Mendoza TR, Nakamura Y, et al: When is cancer pain mild, moderate or severe? Grading pain severity by its interference with function. Pain. 1995;61L277-284.
08/14/12 09:33 AM Chronic pain may be seen as presenting a fundamental challenge to medicine. The experience of chronic pain is very common and chronic pain is part of the experience of many illnesses. However, the links between the experience of chronic pain and visible or detectable pathology or diagnosable illness are often non-existent or unclear. In philosophical terms, chronic pain challenges the distinction between mind and body which much medical knowledge assumes. It also challenges the notion of cure as a goal of medical practice. And we face such patients routinely in our practice. Infact 40% of our total patients constitute pain sufferers. And there is always an urge when talking of pain, to magnify its image, using eye-catching overstatements and graphology and create a larger than life impression. Health care professionals face pain so often; they develop some form of defense mechanism to deal with it. Some learn to ignore it, some play it down and some others dismiss it with a wry smile. But the age old adage remains and shall remain true till science evolves several steps and generations in progress; diagnose as many, treat some, cure a few, but empathize with all.
08/14/12 09:33 AM Pain being such an important presenting complaint in practice, the US government declared the last decade as Decade of Pain Control and Research. This also helped in development of numerous programs to advance awareness and treatment of pain and funding for research.
08/14/12 09:33 AM
08/14/12 09:33 AM Neuropathic pain caused by damage to or a dysfunction of the nervous system e.g. post herpetic neuralgia, diabetic neuropathy, pain following trauma or compression is generally un-diagnosed and poorly managed Nociceptive pain is caused by noxious stimuli of pain receptors with info transferred centrally e.g inflammation or headache, it is managed by analgesics, NSAIDs or opioids
08/14/12 09:33 AM This system is the most comprehensive approach to classification of chronic pain syndromes; it is intended to standardize descriptions of pain syndromes and provide a point of reference. The system establishes a 5-digit code that assigns a unique number to each chronic pain diagnosis. The digital code (1 through 9 within each “axis”) is first, followed by letters used as suffixes, if necessary. Axis I: concerned with regions; if patient has pain in more than one region, use two codes Axis II: concerned with systems, such as nervous system, respiratory, musculoskeletal, etc.; some details open to debate, but practicality should prevail Axis III: deals with characteristics of pain Axis IV : filled in according to the patient’s report of severity or chronicity of the illness Axis V: concerns mechanisms involved in pain production and is most open to debate. Letters (a, b, c, d, etc.): Since some syndromes have same final five-digit code, a letter may be added to the sixth place to distinguish them. It could indicate acute vs chronic conditions, but usually merely indicates the first of several conditions to be described with the same five digits. An example: Mild postherpetic neuralgia of T5 or T 6, 6 months’ duration = 303.22e Axis I: Thoracic region Axis II: Nervous system (central, peripheral, or autonomic); physical disturbance/dysfunction Axis III: Continuous or nearly continuous, fluctuating severity Axis IV: Mild severity of 1 to 6 months Axis V: Trauma, operation, burns, infective, parasitic (one of these) Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:19-21. 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: 3-4.
08/14/12 09:33 AM Complicated by central processing that allows pain to be experienced as a cognitive function.. How we interpret pain is important and can affect patients life- as shown in next slide where the interplay of afferent and efferent fibres is demonstrated.
08/14/12 09:33 AM The physiology of normal pain transmission involves some basic concepts that are necessary in order to understand the pathophysiology of abnormal or nonphysiologic pain. These include the concept of transduction of the first-order afferent neuron nociceptors. The nociceptor neurons have specific receptors that respond to specific stimuli if a specific degree of amplitude of the stimulus is applied to the receptor in the periphery. If sufficient stimulation of the receptor occurs, then there is a depolarization of the nociceptor neuron. The nociceptive axon carries this impulse from the periphery into the dorsal horn of the spinal cord to make connections directly, and indirectly, through spinal interneurons, with second-order afferent neurons in the spinal cord. The second-order neurons can transmit these impulses from the spinal cord to the brain. Second-order neurons ascend mostly via the spinothalamic tract up the spinal cord and terminate in higher neural structures, including the thalamus of the brain. Third-order neurons originate from the thalamus and transmit their signals to the cerebral cortex. Evidence exists that numerous supraspinal control areas—including the reticular formation, midbrain, thalamus, hypothalamus, the limbic system of the amygdala and the cingulate cortex, basal ganglia, and cerebral cortex—modulate pain. Neurons originating from these cerebral areas synapse with the neuronal cells of the descending spinal pathways, which terminate in the dorsal horn of the spinal cord. Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59.
08/14/12 09:33 AM Expand on neural plasticity here – changes in chronic pain vs acute pain is important
08/14/12 09:33 AM Medication acts on different areas of this pathway Ask the audience what medication is effective at each Here we can add in the five points to pain NSAIDs at periphery mostly Paracetamol – or acetaminophen centrally Opioids on ascending pathways interfere with sP A beta fibres affecting gating of pain in S G – T cells Descending pathways also affect T cells in SG
08/14/12 09:33 AM Chronic pain is not just a prolonged version of acute pain. It often occurs in the absence of ongoing illness or after healing is completed, and often begins with an injury that causes inflammation and CNS changes. The injured area heals, scar tissue is formed, and the inflammation recedes. But for an unknown reason, the nervous system undergoes multiple changes that perpetuate the pain experience, continuing to send pain signals to somatic muscles. The nervous system reacts to the memory of the original injury and sends signals like those sent in response to that original injury. These signals become a recurring and disabling message that remind the patient of the original injury. As pain signals are repeatedly generated, neural pathways undergo physiochemical changes that make them hypersensitive to the pain signals and resistant to antinociceptive input. The pain signals can become embedded in the spinal cord, like a painful memory. This is why the c urrent perception of pain can be influenced by prior experience of chronic pain. Marcus D. Treatment of nonmalignant chronic pain. Am Fam Physician. 2000;61:1331-1338; 1345-1346.
08/14/12 09:33 AM Effective management of pain relies on a comprehensive assessment that defines the characteristics, etiology, and the underlying pathophysiology of the pain. Etiology. Defining the underlying organic activity that may be contributing to the pain may clarify the nature of the disease, indicate a prognosis, or suggest the use of specific therapies. Pathophysiology. Animal and clinical research suggest that the clinical presentation and the response to therapy of a particular pain syndrome may be determined by factors linked to the underlying mechanism of the pain. Although the classification that can be derived from such observations may be oversimplistic, it has clinical utility and so has become widely accepted. Using this scheme, the predominating pathophysiology of pain can be broadly defined as nociceptive, neuropathic, and idiopathic. Characteristics. The patient should be asked to describe the characteristics of the pain in terms of temporal aspects, intensity, topography, and exacerbating/relieving factors. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:11.
08/14/12 09:33 AM Nociceptive pain is presumably related to ongoing activation of primary afferent neurons responsive to noxious stimuli. The activation of the nociceptors is related to tissue damage, although the relationship between pain and tissue damage is neither uniform nor constant. Nociceptive pain includes somatic pain and visceral pain. Somatic pain refers to ongoing activation of somatic afferent neurons. Bone pain is a typical example of this type of pain. Visceral pain is related to the activation of the primary afferent neurons that innervate viscera. Liver capsular pain is an example of visceral pain. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:581. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:11. Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain, 3 rd Ed., Baltimore, Lippincott Williams Wilkins , 2001. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:219-247.
08/14/12 09:33 AM Neuropathic pain is believed to be sustained by aberrant somatosensory processing in the peripheral or central nervous system. It includes numerous clinical entities, which vary in their presentation pathophysiology and treatment. The classification is based on inferred location of the pain “generator” (peripheral or central) and types of mechanisms involved. Three major categories have been recognized: deafferentation pain, sympathetically-maintained pain and peripheral neuropathic pain. Deafferentation pains are presumably related to pathophysiologic processes in the CNS. Subtypes include pain caused by injury to the brain or spinal cord, phantom pain, postherpetic neuralgia and pain caused by root avulsion. Sympathetically-maintained pain is defined as a pain presumed to be sustained by efferent activity in the sympathetic nervous system. A sympathetic nerve block is needed to establish the diagnosis of sympathetically-maintained pain. This type of pain appears to occur most frequently in the setting of a complex regional pain syndrome. The term complex regional pain syndrome (CRPS), also known as reflex sympathetic dystrophy or causalgia , refers to a regional pain syndrome in which pain is associated with focal autonomic dysfunction (vasomotor instability, swelling, sweating) and/or trophic changes (thinning of the skin, changes in hair growth, bone and subcutaneous tissue losses). Peripheral neuropathic pain is usually caused by a focal peripheral nerve injury or by a diffuse injury (polyneuropathy). Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:83, 87, 93.
08/14/12 09:33 AM Idiopathic pain persists in the absence of an identifiable organic substrate and is believed to be excessive for the organic processes that exist. This type of pain is uncommon in mentally ill patients. A subgroup of patients with idiopathic pain presents positive evidence of a predominant psychologic contribution to the pain. These pains are described as psychogenic or are labeled with a specific psychiatric diagnosis. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:19-21. 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. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:11.
08/14/12 09:33 AM Since the early 1960’s, developments have taken place that can rectify some of the deficiencies in the understanding and treatment of pain that existed even in the early 20 th century. Research has given us a greater understanding of the pathophysiology underlying many chronic pain syndromes. This understanding has led to advances in drug therapies, the use of multimodal therapies, and the belief that in some cases the optimal treatment of chronic pain is best managed by a multidisciplinary team. A pioneer and giant in the field of pain therapy, John Bonica, established the first multidisciplinary pain clinic, the Multidisciplinary Pain Center, at the University of Washington in 1960. Patient’s rights movements have been supported by documents such as the Joint Commission on Accreditation of Healthcare Association’s (JCAHO) Pain Standards for 2001 , which states that all patients have the right to the appropriate assessment and management of pain. Joint Commission on the Accreditation of Healthcare Organizations. Patient Rights and Organization Ethics. Referenced from the Comprehensive Accreditation Manual for Hospitals, Update 3, 1999. http://www.jcaho.org/standards_frm.html Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:3-15.
08/14/12 09:33 AM Numerous surveys from the United States and Europe during the last decade have shown that 30% to 50% of adult patients in active therapy for a solid tumor experienced chronic pain. With advanced disease, the prevalence of pain increased to 90%. A recent survey by the IASP concluded that the inferred mechanism of pain is neuropathic in 40% of cases. In a very large survey of institutionalized elderly patients with cancer, the prevalence of pain was 27.4%, and pain was associated independently with age, gender, race, marital status, functionality, and cognitive status. Cancer pain is often associated with psychological distress and functional impairment. Unrelieved pain may significantly impaired quality of life . In the AIDS population, the prevalence rates range from 25% to 80%. This broad range reflects differences in populations studied and pain assessment methodologies. Bernabei R, Gambassi G, Lapane K, et al: Management of pain in elderly patients with cancer. JAMA. 1998;279:1877-1882. Caraceni A, Portenoy RK, a working group of the IASP Task Force on Cancer Pain. An international survey of cancer pain characteristics and syndromes. Pain . 1999;82:263-274. Cleeland CS, Gonin R, Harfield AK, et al: Pain and its treatment in outpatients with metastatic cancer. N Engl J Med. 1994;330:592-596. Heim HM, Oei TP: Comparison of prostate cancer patients with and without pain. Pain. 1993; 53:159-162. Portenoy, RK: Cancer pain. Pathophysiology and syndromes. Lancet. 1992; 339:1026-1031. Portenoy RK, Kornblith AB, Wong G, et al: Pain in ovarian cancer. Prevalence, characteristics, and associated symptoms. Cancer . 1994;74:907-915. Serlin RC, Mendoza TR, Nakamura Y, et al: When is cancer pain mild, moderate or severe? Grading pain severity by its interference with function. Pain. 1995;61L277-284.
08/14/12 09:33 AM The goal of pain assessment is the development of a pain-oriented problem list, which, in addition to characterizing pain, prioritizes other physical and psychosocial problems that may influence therapy or be amenable to primary treatment. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:563-589.
08/14/12 09:33 AM In order to make a comprehensive evaluation, the physician must take a detailed history from the patient. Temporal Features. Temporal features include onset, duration, frequency and constancy of the pain. Pain can be acute or chronic. Chronic pain may be punctuated by breakthrough pains (transitory acute pain). Intensity. Pain intensity should be measured validly and repeatedly using a simple scale. (See next slide) Topography. Pain can be described as focal, multifocal, generalized, referred. Focal pain s are usually well circumscribed, at the site of the lesion. Referred pains are experienced at a site remote from the presumed lesion. Pains can be referred from an injury in any deep tissues, including viscera, muscle, bone and peripheral or central nervous system. Quality. Descriptors of pain quality can be clues to underlying mechanisms. Somatic pains are often described as aching, throbbing or sometimes stabbing. The quality of visceral pains will vary according to the organ. In injury to hollow viscus, the pain is often described as cramping or gnawing. Neuropathic pains are usually described as dysesthesic (lancinating, burning, electric-shock-like, tingling). Exacerbating/Relieving Factors. Factors that aggravate or relieve pain may be useful for diagnostic purposes and treatment: they can be categorized as volitional or spontaneous. Pain induced by light touch on normal skin (allodynia) suggests a neuropathic component. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse, 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:566-567.
08/14/12 09:33 AM A “faces” scale may be useful for patients who are unable to use NRS or VAS scales, such as children, the elderly, or patients with dementia. The Brief Pain Inventory is a straightforward and easily administered tool that provides the practitioner with information about pain history, intensity, location, quality, and interference. It includes a number of questions, each of which is answered by the patient on a scale of 1 to 10. Included are questions about pain characteristics as well as functionality. It also includes the simple body outlines above, on which the patient is asked to mark the areas of greatest pain. Cleeland, CS. Pain Research Group University of Texas M.D.Anderson Cancer Center. BPI Copyright 1991. Wong DL, Hockenberry-Eaton M, Wilson D, Winkelstein ML, Schwartz P. Wong’s Essentials of Pediatric Nursing. 6 th ed. St Louis, Missouri: Mosby, Inc.; 2001:1301. Reprinted by permission .
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08/14/12 09:33 AM Opioid Analgesics . Opioids are the mainstay drugs for moderate-to-severe pain associated with medical illness. Opioid analgesics can be classified as pure mu-agonists or agonist-antagonists based on their receptor interactions. The agonist-antagonist class can be subdivided into a mixed agonist-antagonist subclass and a partial agonist subclass. Because of their ceiling effect for analgesia and potential for reversing analgesia from pure agonists in physically-dependent patients, the agonist-antagonist drugs are not preferred for treating chronic pain. Nonopioid Analgesics. N onopioid analgesics include acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDS). They are usually used for mild-to-moderate pain. They have an additive effect when combined with opioids. There is substantial variability in the response of individual patients to different drugs. The selective COX-2 inhibitors (celecoxib, rofecoxib, valdecoxib, oncloxicam) have a more favorable GI safety profile than the nonselective COX-1 and COX-2 inhibitors. The nonselective drugs vary in toxicity. Drug selection should be influenced by drug-selective toxicities, prior experience, cost, and convenience. Adjuvant Analgesics. Adjuvant analgesics are drugs that have other primary indications but may be analgesic in specific circumstances. In the medically ill, adjuvant analgesics are more commonly used in the treatment of neuropathic pain. Drug selection should be guided by the risks associated with the therapy and the possibility of secondary benefits for symptoms other than pain. Sequential trials and dose titration are usually necessary. The appropriate use of adjuvant analgesics requires the clinician to know the approved indications, side effects, time-action relationship, pharmacokinetics, and specific guidelines for use in pain treatment. Cashman JN. The mechanisms of action of NSAIDS in analgesia. Drugs. 1996;52(suppl 5):S13-S23 . Galer BS. Painful poplyneuropathy. Neurologic Clinics. 1998;16(4):791-811. Hanks GW, Portenoy RK, MacDonald N, et al. Difficult pain problems. In: Doyle D, Hanks GW, MacDonald N, eds. Oxford Textbook of Palliative Medicine . Oxford: Oxford University Press; 1998:454. Langman MJ, Jensen DM, Watson DJ, et al. Adverse upper gastrointestinal effects of rofecoxib compared with NSAIDs. JAMA. 1999;282:1929-1933. Simon LS, Weaver AL, Graham DY, et al. Anti-inflammatory and upper gastrointestinal effects of celocoxib in rheumatoid arthritis: a randomized controlled trial. JAMA. 1999;282:1921-1928. Stein C. The control of pain in peripheral tissues by opioids. N Engl J Med. 1995;332:1685-1690.