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    Al-Azhar UniversityGAZA

    Palestine Faculty of Medicine

    Pain Management

    Prepared by :Ghady Shatat

    Fatma Shnewra

    Haneen Abu Aqlain

    Salwa Al-Khozendar

    3ndyear students

    May , 2013

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    Pain Management

    What is pain?

    Pain has been defined as: an unpleasant sensory and emotional

    experience associated with actual or potential tissue damage, or

    described in terms of such damage

    American Pain Society (APS) has coined the phrase, Pain: the 5th

    vital sign.To underscore the importance of pain monitoring andmanagement in patients.

    Pain is completely subjective and cannot be proved or disproved.

    Pain is whatever the experiencing person says it is, existing whenever

    the experiencing person says it does .

    Pain is very complex. It is both a sensory and emotional experience.

    Substances used in pain:

    Neuroscientists know quite a bit about the mechanisms of pain.

    There are a number of things that promote pain:

    Substance P, Excitatory aminoacids, Prostaglandins, Kinins, Nerve growth

    factor, Cytokine, corticotrophin-releasing hormone.

    We know about elements that attenuate pain :

    Descending antinociceptive pathways, opioids and opioid receptors,

    gamma-aminobutyric acid (GABA), cytokines, and CRH.

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    Factors that Influence Pain perception

    What is Pain perception defined as?

    The process by which pain is recognized and interpreted by thebrain.

    Subjective and dependent on the conditioning of the individual.

    What are factors that influence perception of pain?

    Biological factors that can vary pain perception include the persons

    sex, genetics and number of nociceptors, or pain receptors in the body.

    Social and cultural factors influencing pain intensity might include anexpectation that pain is something you just deal with (less likely to

    communicate pain) and an overly solicitous family caregiver (more likely

    to communicate pain).

    Some psychological issues that can worsen pain follow:

    Fear of pain, which can lead to a patient not moving, especially when a

    certain movement caused pain in the past

    Pain catastrophizing an inability to stop thinking about ones pain

    and to characterize pain as unbearable, which increases activity in areas

    of the brain related to anticipation of pain, according to several studies

    Negative affect (neuroticism) a more irritable or anxious personality,

    which may be a precursor to pain-related fear or catastrophizing

    Depression

    Emotional stress

    Gender and Genetics

    Types of pain:According to pain duration,

    There are 2 types of pain:

    Acute pain:

    It is relatively brief in duration(less than 30 day), and is usually due to

    trauma, surgical procedure, or a specific disease process.usually self

    limiting as the initial injury heal

    Increase ANS activity usually accompany acute pain (tachycardia

    ,tachypnea , HTN, mydriasis and diaphoresis)

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    Chronic pain:

    may last for years. It usually accompanies a chronic, persisting

    clinical entity -- rheumatoid arthritis, osteoarthritis, or back pain..

    Chronic pain can be quite disabling, often preventing people from

    working and enjoying life. It can lead to people feeling isolated,

    angry, frustrated, and guilty

    chronic cancer pain:

    Pain in cancer survivors iccurs in (60-90)% of cancer patients .

    it is caused by residual tissue damage from the cancer and/or the

    cancer therapy.

    Breakthrough pain:

    Breakthrough pain is pain that comes on suddenly for short periods oftime

    [and is not alleviated by the patients' normal pain management. It iscommon incance rpatients .

    Forexample , If you takegabapentin for nerve pain, but suddenlyexperience additional shooting pains, you could be having breakthrough

    pain.

    According to Pain Intensity:Can be broadly categorized as: mild,moderate and severe. It is common to use a numeric scale to rate painintensity where 0 = no pain and 10 is the worst pain imaginable:

    Mild: 7/10

    Accodding to pathogenesis:

    Nociceptive: represents the normal response to noxious insult or injuryof tissues such as skin, muscles, visceral organs, joints, tendons, orbones.

    Examples include:

    Visceral: hollow organs and smooth muscle; usually referred

    http://en.wikipedia.org/wiki/Cancerhttp://drugsaz.about.com/od/drugs/gabapentin.htmhttp://drugsaz.about.com/od/drugs/gabapentin.htmhttp://en.wikipedia.org/wiki/Cancer
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    Neuropathic: pain initiated or caused by a primary lesion or disease inthe somatosensory nervous system.

    o Sensory abnormalities range from deficits perceived as numbnessto hypersensitivity (hyperalgesia or allodynia), and to paresthesias

    such as tingling.

    o Examples include, but are not limited to, diabetic neuropathy,postherpetic neuralgia, spinal cord injury pain, phantom limb (post-amputation) pain, and post-stroke central pain

    Somatic: musculoskeletal (joint pain, myofascial pain),cutaneous; often well localize

    Principles of management.

    Regularly screen all patients for pain and perform a comprehensive pain

    assessment when pain is present.

    Appropriate pain management target.

    Individualised pain management regimens.

    Monitoring of pain management regimens and reassessment of patients

    pain.

    Limitations to pain management:

    Despite the increased focus on pain management and the implementation of

    formal guidelines and standards for the management of pain, a significant

    number of patients continues to experience unacceptable levels of pain.

    Different factors interfere with proper management of pain; some of them

    related to the patient, others related to the health care providers, and some to

    the organizational system.

    Patient :

    Some patients don't tell the doctor about their real pain because they are

    afraid from the injections and drugs or they think that increasing the pain

    sensation means the disease is getting worse.

    Socioeconomic factors.

    Cultural and religious issues.

    Care provider :

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    Inadequate knowledge and formal training in acute pain management.

    Opiophobia.

    System:

    Lack of standard pain control system.

    Hospital policies regarding drug administration and resources available.

    So for effective pain management , barriers should be recognized, addressed

    and overcome.

    Useful Questions in Assessing Pain:

    Onset:

    When did it begin? How often does it occur? How long does it last?

    Exacerbating or relieving factors:

    What brings it on? What makes it better? What makes it worse? Is the pain

    better lying down or standing up? Is it worse on movement?

    Localization, Region and Radiation:

    Where is the pain? Does it move anywhere? Is there more than one site?

    Quality:

    What does it feel like? Can you compare it to anypain youve hadbefore?

    Severity:

    How intense is your pain? At best? At worst? On average? How bothered

    are you by the pain? Are there any other symptoms that accompany the pain?

    Understanding and Impact:

    What does the pain stop you doing? How are you sleeping? What do you

    think is causing the pain? What is your goal for the pain? Are there any other

    views or feelings about the pain that are important to you and your family?

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    Management of pain :

    1-Non pharmacological2- Pharmacological

    1) Non pharmacological :

    Non-pharmacological therapies are ways to decrease pain in addition to

    medicine. Each person may respond to these therapies differently.

    Heat Therapy:

    Works through vasodilation, which is when blood flow increases in the

    injured area due to the heat. The blood increases nutrients and oxygenin the area. It also increases the range of motion in muscles and joints,

    while reducing the likelihood of muscle spasms. Apply heat to the area

    for 20 to 30 minutes every 2 hours for as many days as directed.

    Heat can be used to relieve pain caused by chronic conditions of the

    muscles and joints, such as:

    Arthritis

    Old sprains or strains

    Muscle spasmsMuscle stiffness

    Heat is best for injuries or conditions that are not in the acute phase. In

    other words, it not used on a fresh injury: this could increase swelling,

    which in some cases could increase patient's discomfort. In these cases,

    ice is a better choice. Also, don't apply heat over irritated skin or open

    wounds (including incisions that are still healing). Finally, people with

    cancer should not use heat to treat pain, as there is a chance of

    increased tumor growth.

    Ice Therapy:

    When ice is applied to the skin, it has a few different effects on the

    surrounding tissues. First, it partially numbs the area, which can help

    temporarily reduce pain. Second, it causes blood vessels to tighten,

    which decreases the blood flowing into the area. In this way, ice can

    help decrease swelling and even slow or stop bleeding. In some cases,

    applying ice to the skin may even prevent some bruising.

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    Ice can be beneficial for anyone who has a chronic pain condition that

    causes (or is caused by) inflammation. Some of the conditions we

    recommend ice for in our therapy clinic include:

    Carpal tunnel syndrome

    Migraine headaches

    Trigeminal neuralgia

    Tendinitis

    Arthritis

    Massage Therapy:

    Researchers at McMaster University in Canada found that massage

    affects the activity of certain genes, directly reducing inflammation in

    muscles - the same result youd get by taking aspirin or ibuprofen - and

    boosting their ability to recover from exercise.

    Researchers found that massage set off a series of molecular events in

    muscles that helped reverse discomfort related to exercise. Massage

    dampened the activity of proteins known as inflammatory cytokines,

    which cause inflammation and pain. It also increased levels of proteins

    that signal the muscles to produce more mitochondria, the cell structures

    that produce energy and help muscles recover from activity.

    Aromatherapy: This is a way of using scents to relax, relieve stress,and decrease pain. Aromatherapy uses oils, extracts, or fragrances fromflowers, herbs, and trees. They may be inhaled or used duringmassages, facials, body wraps, and baths. . Aromatherapy is effectivebecause it works directly on the amygdala, the brains emotional center,says Mehmet Oz, MD, professor of surgery at Columbia UniversityMedical Center in New York City.

    Guided imagery: This teaches you ways to put pictures in your mindthat will make pain less intense. It may help you learn how to change theway your body senses and responds to pain.

    Laughter: Laughter may help you let go of stress, anger, fear,depression, and hopelessness.

    Music:This may help increase energy levels and improve your mood. Itmay help reduce pain by triggering your body to release endorphins.These are natural body chemicals that decrease pain.

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    Biofeedback: This teaches your body to respond differently to thestress of being in pain. Caregivers may use a biofeedback machine tohelp you know when your body is relaxed.

    Self-hypnosis:This is a way to direct your attention to something otherthan your pain. For example, you might repeat a positive statementabout ignoring the pain or seeing the pain in a positive way.

    Acupuncture: This therapy uses very thin needles to balance energychannels in the body. This is thought to help reduce pain and othersymptoms.

    Each patient experiences pain differently. It is important to discover the

    best method for pain control for your patient prior to the onset of pain.

    2)Pharmacological :

    In 1988, the World Health Organization (WHO) declared Cancer Pain

    management a worldwide emergency and adopted the Canadian 3-step

    ladder of analgesic agents for control of nociceptive pain.It is NOT a rigid clinical path that must be traversed in the care of every

    patient.

    For mild pain start at step one, for moderate pain step two, for severe

    pain step three. As the severity of pain increases, maximize the dosing

    at the current step and then, if this is insufficient, move up the ladder.

    Step 1:

    Acetaminophen & ASA & NSAIDs

    They obey first order kinetics and may be dosed up to

    recommended maximums .

    Many are available without prescription.

    Sustained release preparations or drugs with longer half-lives may

    encourage adherence.

    Step 2:

    Several opioid analgesics are conventionally available in

    combination with either acetaminophen or ASA and are commonly

    used to manage moderate pain.

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    With the exceptions of propoxyphene (that truly has weak

    analgesic activity), tramadol (that has a unique combination of very

    weak opioid activity with other analgesic properties) and codeine

    (that has 1/10 to 1/12 the potency of morphine), the opioids in this

    class are close in potency to morphine (mg for mg).

    However, they have been termed "weak" opioids because, in

    combination, they have a ceiling to their analgesic potency(i.e. 4

    gm acetaminophen per 24 hours).

    If pain persists, or increases, despite a maximum dose of a step

    two drug, a step three drug should be prescribed instead

    Step 3: The pure agonist opioid analgesics comprise step three of the WHO

    analgesic ladder.

    Morphine is the prototypical drug because of its ease of

    administration and wide availability.

    Many patients with chronic pain are best managed with an

    appropriately titrated strong opioid that is combined with one or more

    coanalgesics.

    In contrast with the step-one and step-2 analgesics, there is noceiling effect or upper limit to the dose of opioids when titrating to

    relieve pain.

    Step 4:

    In general, "step four" involves invasive approaches for pain relief

    that can be summarized as follows.

    Subcutaneous (SC) or intravenous (IV) administration of opioid

    analgesics and coanalgesics may be required for patients where oral(PO), buccal mucosal, rectal (PR), or transcutaneous approaches are

    not possible or practical, or where doses of oral opioids lead to

    undesirable side effects. Side effects may be minimized as a result of

    the uniform delivery of the drug parenterally, the change in route of

    administration or the reduction in first pass metabolite production.

    Subcutaneous administration may be preferable to intravenous

    approaches as it results in equivalent serum levels and analgesia

    without the risks of thrombosis or infection, and is much easier todeliver, for much less cost.

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    Administration of opioid analgesics either epidurally or intrathecally

    may be required in selected patients.

    Intraventricular application of opioid analgesics and other drugs has

    been investigated for selected central pain syndromes.

    Neuroablative techniques such as peripheral neurolytic blockade,

    ganglionic blockade, cordotomy and cingulotomy may be appropriate

    in highly selected patients.

    Acetaminophen (APAP):

    Mechanism of action unclear

    No anti-inflammatory effects

    Causes liver toxicity at high doses

    Max dose: 4 gm/day, if no liver disease

    Newest recommendation 2.6 gm/day

    Decreases opioid requirements

    NSAID& ASA :

    NSAIDs are anti-inflammatory through their ability to inhibit the enzyme

    cyclooxygenase that catalyzes the conversion of arachidonic acid to

    prostaglandins and leukotrienes.

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    Their effect is to decrease the levels of these inflammatory mediators

    that sensitize nerve endings to painful stimuli. Because analgesia from NSAIDs is achieved through a different

    mechanism from the opioids and other adjuvant analgesics, they may becombined with these drugs to achieve better pain relief than with a single

    drug alone.

    Primary analgesia may be achieved at lower doses than those required

    for anti-inflammatory action. Therefore, when used as an adjuvant for

    their anti-inflammatory effects, maximum doses should be used.

    The side effects of the NSAIDs are related to their mechanism of action.

    Inhibition of cyclooxygenase leads to inhibition of platelet aggregation,decreased cytoprotection in the gastric mucosa, and decreased renal

    perfusion. Consequently, bleeding and renal failure are important side

    effects.

    The dyspepsia and abdominal pain that limit use of the NSAIDs in some

    patients do not correlate with significant gastric erosions and

    gastrointestinal bleeding. Similarly, the use of an H2 blocking antacid

    (e.g. cimetidine or ranitidine) to treat NSAID dyspepsia and abdominal

    pain does not prevent gastric erosions and gastrointestinal bleeding.

    Only misoprostol, which reverses the effect of NSAIDs on the micro-

    arteriolar circulation of the stomach, has been shown to heal gastric

    erosions and reduce the risk of significant gastric bleeding In contrast with the opioids, the NSAIDs and acetaminophen have a

    ceiling effect to their analgesic potential, do not produce

    pharmacological tolerance, and are not associated with physical or

    psychological dependence.

    Opioids:

    Originally derived from poppies

    Body possesses endogenous opioids

    enkephalins

    endorphins

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    Opiate Receptors

    mu

    delta

    kappa

    sigma

    The opioid analgesics in common usage may be divided into those

    which are full mu agonists, partial agonists and mixed agonist-

    antagonists. The pure agonist drugs are the most useful in chronic

    intractable pain.

    Side effect of opioids:

    Common side effects of the opioid analgesics are easily managed. In the

    majority of patients, pharmacological tolerance develops to all of the

    common side effects except constipation, within one to two weeks.

    Consequently, nausea and vomiting may be treated expectantly with

    antiemetics for the short period that these symptoms are problematic. If

    nausea and/or vomiting persist, simply changing the opioid or the route

    of administration may resolve the problem.

    Similarly, patients should be counseled that the drowsiness they

    experience when initiating an opioid will usually dissipate after the first

    week or so. Patients can often tolerate a little drowsiness if they are

    assured that it wont persist for the entire time they are taking opioid

    analgesics. In fact, once a stable dose of an opioid has been reached,

    drowsiness will likely settle completely, function will normalize and most

    patients on a stable dose of opioid may safely drive a car. Persistent

    somnolence may be managed by ensuring adequate hydration and renal

    clearance, changing to a sustained release product to minimize peak

    effects, changing the opioid, changing the route of administration or by

    adding a psychostimulant (such as methylphenidate or pemoline). As patients given opioid analgesics will not develop tolerance to

    constipation, they should be treated with cathartic laxatives (e.g. Senna

    or Bisacodyl), osmotic laxatives (e.g. magnesium salts or lactulose) or

    prokinetic agents (e.g. metoclopramide or cisapride) on a routine basis.

    Simple stool softeners (e.g. sodium docusate) are usually ineffective

    Persistent side effects of the opioids seem to be somewhat idiosyncratic

    to the drug and individual. Simply changing to an alternate opioid at anequal analgesic dose will often clear the problem.

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    The uncommon side effects of the opioids are also manageable. The

    dysphoria and confusion that occasionally occur may be managed by

    ensuring adequate hydration and renal clearance (thereby minimizing

    metabolite buildup), lowering the opioid dose, changing the opioid

    analgesic or by adding low doses of a neuroleptic drug such as

    haloperidol, chlorpromazine or risperidone. The pruritus and urticaria that occurs with opioids is not immune

    mediated, but a non-specific release of histamine from mast cells in the

    skin. This may be managed with long-acting antihistamines or by

    changing to an alternative opioid analgesic. True allergy presenting as

    bronchospasm leading to anaphylaxis is extremely rare. Most patients

    who report allergy have had poorly managed side effects (usually

    nausea/vomiting and/or constipation) or too much medication too fast

    (leading to drowsiness and/or confusion).

    The risk of respiratory depression from opioid analgesics in patients with

    pain is frequently misunderstood. Pain is a potent stimulus to breathe

    and a significant stressor. While we cannot be certain of the effects of

    the first dose in an opioid nave patient, patients develop

    pharmacological tolerance to the respiratory depressant effects of

    opioids over the same time course as other side effects. Consequently,

    in the patient taking opioid analgesics for any significant length of time, it

    is difficult to demonstrate significant respiratory depression even with

    large doses of opioids. Too frequently opioids have been withheld or under-dosed because of

    unsubstantiated fear of respiratory depression or the mismanagement of

    side effects. In the patient with uncontrolled pain, narcotic analgesics

    can be judiciously but expeditiously and safely titrated until adequate

    relief is obtained or intolerable side effects encountered.

    Opioid overdose: In the setting of pain management, increasing opioid excess presents

    first as mild drowsiness, proceeds to persistent somnolence, then to a

    poorly arousable state and finally to respiratory depression. These

    changes may be associated with increasing restless, agitation,

    confusion, dreams, hallucinations, myoclonic jerks or even sudden onset

    of seizures.

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    When assessing a patient for respiratory depression, it is important to

    remember that a respiratory rate of 8-12 is frequently normal, particularly

    at nighttime. If early, or even moderate excess is present without major

    compromise, the opioid can be held and normal metabolism will clear

    the excess opioid, particularly if the poorly hydrated patient is adequately

    rehydrated. Naloxone reversal is not normally necessary. If the patient is not arousable, has a respiratory rate less than 6-8 per

    minute or there is significant hypoxemia or hypotension present, opioid

    reversal with naloxone may be warranted. Dilute a 0.4 or 1.0 mg ampule

    of naloxone with 10 cc of saline and administer 0.1-0.2 mg IV boluses

    every 1-2 minutes. Sc or po administration is not appropriate. As

    naloxone has a high affinity for opioid receptors, titration any faster, or

    with larger boluses, may precipitate acute opioid withdrawal that

    presents as an acute pain crisis, psychosis or severe abdominal pain

    and precipitates pulmonary edema or even myocardial infarction. Only if

    several 0.1-0.2 mg boluses are ineffective should the bolus size be

    increased.

    Naloxone has a high affinity for lipids and will redistribute itself into

    adipose tissue within 10-15 minutes of administration. Any improvement

    frequently appears to disappear within this time frame and signs of

    toxicity return. Repeated naloxone dosing may be necessary to sustain

    the reversal until the patient has cleared sufficient of the opioid to be out

    of danger. If the overdose is severe and considerable naloxone is

    required, a continuous infusion of naloxone may be required until the

    crisis is over. If a patient, who has been well managed on a stable dose of opioid for

    some time suddenly develops signs of overdose, the opioid should be

    stopped and sepsis or other causes should be ruled out. It is unlikely

    that the opioid alone will be the cause of the "effective overdose".

    Addict ion and Tolerance: Addiction, the psychological dependence on the drug, is also a vastly

    overrated and misunderstood consequence of using opioid analgesics.

    In patients with chronic pain, the incidence of addiction is less than

    1:1000 and is usually related to preexisting dependency. Because of its

    rarity, it is not listed in Table 1 with the other side effects of the opioids.

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    Physical dependence, meaning the development of a withdrawal

    syndrome upon abrupt discontinuation of the drug, is not evidence of

    addiction. Physical dependence occurs over the same time course as

    tolerance develops to the side effects of the opioid analgesics and is the

    result of changes in the numbers and function of opioid neuro-receptors

    in the presence of exogenous opioid. If opioid analgesics are tapered instead of abruptly withdrawn,

    withdrawal symptoms do not occur. Usually the opioid dose can be

    reduced by 50-75% q2-3days without ill effect. Occasionally a small

    dose of a benzodiazepine (e.g. 0.5-1.0 mg of lorazepam) or of

    methadone (with its longer half-life) may be necessary to settle the

    feeling of slight uneasiness or restlessness that accompanies the

    tapering process. If restlessness or agitation is anything more than very

    mild, the rate of tapering should be slowed.

    Adjuvant analgesics:

    Adjuvant analgesics are drugs used to enhance the analgesic efficacy of

    opioids, treat concurrent symptoms that exacerbate pain, and/or provide

    independent analgesia for specific types of pain. They may be used in all

    stages of the analgesic ladder. Some of the adjuvants, such as

    acetaminophen, the NSAIDs, the tricyclic antidepressants and perhaps

    the antiepileptics have primary analgesic activity themselves and may be

    used alone or as coanalgesics.

    Two cancer pain syndromes bear particular mention in this regard. Bone

    pain from bone metastases is thought to be, in part, prostaglandin

    mediated. Consequently, the NSAIDs and/or steroids may be particularly

    helpful in combination with opioids. Cord compression should always be

    considered if the pain is severe, increasing quickly or associated with

    motor, bowel or bladder dysfunction. Neuropathic pain is rarely controlled with opioids alone. The tricyclic

    antidepressants, antiepileptics and steroids are often required in

    combination with the opioids to achieve adequate relief. Commonly used

    agents are listed below with a few comments about their use NSAIDs and/or acetaminophen may be added to the opioids for adjuvant

    analgesia, particularly when inflammatory or peripheral mechanisms are

    thought to be responsible for the painful stimulus.

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    Corticosteroids provide a range of effects including anti-inflammatory

    activity, mood elevation, antiemetic activity and appetite stimulation.

    They reduce pain both by their anti-inflammatory effect of reducing

    arachidonic acid release to form prostaglandins as well as decreasing

    swelling and pressure on nerve endings. Undesirable effects such as

    hyperglycemia, weight gain, myopathy, and dysphoria or psychosis may

    complicate prolonged therapy. Anticonvulsants (such as carbamazepine, valproate, clonazepam,

    phenytoin, and gabapentin) are used either alone, or in addition to

    opioids or other coanalgesics to manage neuropathic pain. They have

    been particularly advocated for neuropathic pain with a shooting or

    lancinating quality (such as trigeminal neuralgia or nerve root

    compression).

    Tricyclic antidepressants (such as amitriptyline, desipramine,

    imipramine, nortriptyline) are useful in pain management in general, and

    neuropathic pain in particular. They have innate analgesic properties

    and are effective through mechanisms that include enhanced inhibitory

    modulation of nociceptive impulses at the level of the dorsal horn. If the

    anticholinergic side effects of tertiary amine tricyclics (amitriptyline,

    imipramine) are undesirable or troublesome, the secondary amine

    tricyclics (nortriptyline, desipramine) may be effective analgesics and

    produce fewer side effects. The selective serotonin reuptake inhibitor

    class of antidepressants has not been shown to be useful in similar ways

    to the tricyclic antidepressants. Bisphosphonates (such as pamidronate) and calcitonin have been used

    as adjuvant analgesics in the management of bone pain from bone

    metastases. In cancer, bone pain is caused in large part by osteoclast-

    induced bone resorption rather than the direct effects of the tumor on

    periosteal or medullary nerve endings. Both the bisphosphonates and

    calcitonin inhibit osteoclast activity on bone and have been reported to

    reduce pain significantly in at least some patients.

    Neuroleptic medications (such as haloperidol, chlorpromazine or

    risperidone) and anxiolytics (such as lorazepam) are used for the

    management of specific psychiatric disorders that complicate pain

    management such as delirium, psychosis, or anxiety disorders. With the

    exception of methotrimeprazine and clonazepam, none have been

    shown to have intrinsic analgesic activity.

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    Symptoms of Pain in Babies:

    Unlike with older children, crying isn't always a reliable pain indicator in

    babies. That's because crying is a baby's way of expressing a wholehost of needs. Here are signs that a baby may be in pain.

    Changes in crying patterns. A baby's distressed cry sometimes, but not

    always, sounds different from ordinary crying. Changes in your baby's

    behavior can also be a tip-off. For example, crying that can't be soothed

    with a bottle, diaper change, or cuddling could signal pain. Also, a calm

    baby who becomes unusually fussy could be in pain.

    Crying while nursing. Sucking can create pressure in the ears. The baby

    who cries while nursing could very well have a painful ear infection. Prolonged, intense crying, often at the same time each day. This

    behavior is common with colic, which occurs in infants due to abdominal

    pain. It often starts at the age of 2 weeks, peaks at 6 weeks, and then

    gradually declines.

    Crying and drawing the legs up to the abdomen. Your baby could have

    colic or a serious medical condition.

    Withdrawing. Chronic pain can sap a baby's energy, causing him or her

    to become still, quiet, and to avoid eye contact.