chronic pain: role of tricyclic antidepressants, dolsulepin

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  • Chronic pain: Core concepts and TCAsDR SUDHIR KUMAR MD (Med) DM (Neuro)CONSULTANT NEUROLOGISTAPOLLO HOSPITALS, KUKATPALLY/JUBILEE HILLS (HYDERABAD)

  • Consensus statement on Role of tricyclic Antidepressants in chronic neuropathic pain In India

    Endorsed by Indian society for the study of pain (Indian chapter for the study of chronic pain)

  • Existing Guidelines in Neuropathic Pain

    Mechanism and Pharmacokinetics of Tricyclic Antidepressants: The Number Needed to Treat and Number Needed to Harm

    Current Status of Tricyclic Antidepressants in Tension-type Headache.

    Adverse Effects of Tricyclic Antidepressants

    Tricyclic Antidepressants in Cancer Pain and Chemotherapy-induced Neuropathic Pain

    Tricyclic Antidepressants in Painful Polyneuropathy Persistent Idiopathic Facial Pain and Trigeminal Neuralgia

    Central Neuropathic Pain Syndromes

    Current Status of Tricyclic Antidepressants in Post-surgical, Post-traumatic and Phantom Limb Pain

    Drug Interactions of Tricyclic Antidepressants with Various Other Analgesics used in Chronic Pain and Cancer Pain12345678910Salient Features Mentioned in the Guidelines

  • Objectives To effectively and responsibly prescribe TCAs and enhance the quality of life, in patients of chronic neuropathic pain in IndiaTricyclic antidepressants is one of the foremost and first-line Therapies being prescribed for management of chronic neuropathic pain across the globeBut there are no current best practice drug status Guidelines on TCA drug class in India, and hence this is an initiative To put a consensus-based review on the same, with regard to pain practices in India

  • IntroductionKodiath MF. A Comparative Study of Patients with Chronic Pain in India and the United States. Clin Nurs Res August 1992 vol. 1 no. 3 278-291 Pain is the most frequently reported symptom in the health care industry today

    Chronic pain in the US costs millions of dollars annually, and its financial impact is mounting

    Affects nearly all normal activities and often leaves the person feeling helpless and hopeless

  • Pain: Good or bad ?Not all pain is a disease

    Protector to us most of the time.

    Acute pain constitutes a signal to a conscious brain about the presence of noxious stimuli and/or ongoing tissue damage.

    This acute pain signal is useful and adaptive, warning the individual of danger and the need to escape or seek help.

    JL Henry. The need for knowledge translation in chronic pain. Pain Res Manage 2008;13(6):465-476.

    *Not all pain is a disease. Pain is a protector to us most of the time, at least for those of us who do not live with constant pain. Acute pain, such as that following trauma or surgery, constitutes a signal to a conscious brain about the presence of noxious stimuli and/or ongoing tissue damage. This acute pain signal is useful and adaptive, warning the individual of danger and the need to escape or seek help. Acute pain is a direct outcome of the noxious event, and is reasonably classified as a symptom of underlying tissue damage or disease. When the original disorder resolves, so do its symptoms.

    For some, though, pain is a constant companion, persisting long after its usefulness as an alarm signal has passed, and indeed, often long after the tissue damage has healed. Chronic pain in these patients may not be directly related to their initial injury or disease condition, but rather to secondary changes including some that occur in the pain detection system itself.

  • Chronic pain as a disease !

    Pain is a major healthcare problem worldwide. Although acute pain may reasonably be considered a symptom of disease or injury, chronic and recurrent pain is a specific healthcare problem, a disease in its own right

    - The European Federation of International Association for the Study of Pain Chapters

  • Chronic pain - DefinitionSmith BH. Chronic pain in primary care. Fam Pract. 1999 Oct;16(5):475-82.The International Association for the Study of Pain (IASP) defines pain as an unpleasant sensory and emotional experience with actual or potential tissue damage or described by patients in terms of such damageThe IASP defines chronic pain as pain which has persisted beyond normal tissue healing time, taken in the absence of other criteria, to be 3 months

  • Chronic pain - PrevalenceIn a random survey of 2012 Canadians, chronic pain was reported by 29% of respondents, with increased frequency in women and older age groups.

    The average duration of pain was 10.7 years

    The average intensity was 6.3 on a 10-point scale

    Almost 70% of those reporting pain were worried about addiction

    Moulin DE, Clark AJ, Speechley M, Morley-Forster PK. Chronic pain in Canada prevalence, treatment, impact and the role of opioid analgesia. Pain Res Manage 2002;7:179-84.

    *Thirteen primary studies were systematically reviewed. CP prevalence estimates varied widely in studies that used the International Association for the Study of Pain definition of CP (weighted mean: 35.5%, range: 10.5% to 55.2%). In studies that used the criteria of the American College of Rheumatology (ACR) to determine the prevalence of chronic widespread pain, variation was narrower (weighted mean: 11.8%, range: 10.1% to 13%).

  • Chronic pain - CausesChronic pain can arise from sundry causes.Some of the more common types of chronic pain include those of Osteoarthritis, rheumatoid arthritisLow backShoulder and neckHeadache (including migraine)Myofascial pain syndromesChronic regional pain syndromesStump and phantom limb painNeuropathic pain, herpes zoster (shingles) and postherpetic neuralgia, trigeminal neuralgiaDiabetic neuropathyChronic visceral pain syndromes, and others.

    JL Henry. The need for knowledge translation in chronic pain. Pain Res Manage 2008;13(6):465-476.

  • Chronic Pain - PathophysiologyThe mediators of painH+K+Substance PBradykinin5HTPhospholipids & Prostaglandins

    Harrison's Principles of Internal Medicine (17th Edition).New York, NY, USA: McGraw-Hill Professional Publishing, 2008.

    *A. Direct activation by intense pressure and consequent cell damage. Cell damage induces lower pH (H + ) and leads to release of potassium (K + ) and to synthesis of prostaglandins (PG) and bradykinin (BK). Prostaglandins increase the sensitivity of the terminal to bradykinin and other pain-producing substances. B. Secondary activation. Impulses generated in the stimulated terminal propagate not only to the spinal cord but also into other terminal branches where they induce the release of peptides, including substance P (SP). Substance P causes vasodilation and neurogenic edema with further accumulation of bradykinin. Substance P also causes the release of histamine (H) from mast cells and serotonin (5HT)from the platelets.

  • Pain transmission and modulatory pathwaysHarrison's Principles of Internal Medicine (17th Edition).New York, NY, USA: McGraw-Hill Professional Publishing, 2008.A. Transmission system for nociceptive messages.B. Pain-modulation network

    *A. Transmission system for nociceptive messages. Noxious stimuli activate the sensitive peripheral ending of the primary afferent nociceptor by the process of transduction. The message is then transmitted over the peripheral nerve to the spinal cord, where it synapses with cells of origin of the major ascending pain pathway, the spinothalamic tract. The message is relayed in the thalamus to the anterior cingulate (C), frontal insular (F), and somatosensory cortex (SS).B. Pain-modulation network. Inputs from frontal cortex and hypothalamus activate cells in the midbrain that control spinal pain-transmission cells via cells in the medulla.

  • Ascending pain pathways

  • Circuit of pain modulatory pathway.Marks DM. Serotonin-Norepinephrine Reuptake Inhibitors for Pain Control: Premise and Promise. Current Neuropharmacology, 2009, 7, 331-336

    *The CNS pathway responsible for inhibition of pain sensation includes projections from various brainstem nuclei to the spinal cord dorsal horn via the dorsolateral funiculus (DLF). More specifically, DLF fibers are comprised of serotonergic projections from the raphe nuclei, dopaminergic projections from the ventral tegmental area (VTA), and noradrenergic projections from the locus coeruleus. These descending fibers suppress pain transmission at the nociceptive spinal cord neurons presumably by hyperpolarizing afferent sensory neurons using endogenous opioids, or serotonin and norepinephrine as principal inhibitory mediators.

  • Chronic pain processesNeurogenic inflammation

    Damaged nerve

    Sensitization

    Loss of nociceptive control

    Mental overload

    Whitten, Christine, MD, Donovan, Marilee, RN, PhD, Cristobal, Kristene, MS. Treating Chronic Pain: New Knowledge, More Choices. Clinical Contributions. The Permanente Journal. Fall 2005. Vol. 9. No. 4. Retrieved: January 15, 2006 from: http://xnet.kp.org/permanentejournal/fall05/pain3.html.

    *NEUROGENIC INFLAMMATION Increased prostanoid production at site of pain produces allodynia and hyperalgesia and generates spontaneous pain.DAMAGED NERVE Damaged sensory nerves may send constant pain signals like an alarm bell that wont shut off.SENSITIZATION Repeated pain signals produce changes in the nervous system called WINDUP. Pain becomes more painful.LOSS OF NOCICEPTIVE CONTROL Normally innocuous stimuli become painful. Once activated, any movement/deformity of tissues becomes painful.MENTAL OVERLOAD Possible neurochemical link between pain and memory. High incidence of depression, anxiety. Suffering increases perceived pain.

  • Chronic pain mechanismsWhitten, Christine, MD, Donovan, Marilee, RN, PhD, Cristobal, Kristene, MS. Treating Chronic Pain: N

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