Pain pathways

Pain is the common symptom in many chronic conditions such as cancers, neuropathies, and chronic disease. It is also experienced in trauma varying from mild to severe based on the location and degree of trauma. This presentation is a brief outline on types of pain, classification of pain, pain pathways and management of pain

1. PAIN PATHWAYS & PAIN MANAGEMENT

2. DEFINITION The word pain is derived from the L atin word Peone and the Greek word Poine meaning penalty or punishment Pain is defined by The International Association for the Study of Pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. (or) Pain is an unpleasant subjective experience that is the net effect of a complex interaction of the ascending and descending nervous systems involving biochemical, physiologic, psychological and neocortical processes

3. HISTORY ARISTOTLE considered pain a feeling and classified it as a passion of the soul, where the heart was the source or processing centre of pain DESCRATES, GALEN, VESALIUS postulated that pain was a sensation in which brain played an important role In 19 th century, MUELLER, VAN FREY, GOLDSCHEIDER hypothesized the concepts of neuroreceptors, nociceptors, and sensory input

4. EPIDEMIOLOGY According to The American Pain Foundation, more than 50 million people in the US suffer from chronic pain. An additional 25%, 20 million experience acute pain from injury or surgery The annual incidence of moderate – intensity back pain is 10% - 15 % in the adult population with a point prevalence of 15% - 30% The National Institute for Occupational Safety and health estimated that the cost of low back pain alone was between 50 billions – 100 billions per year

5. CLASSIFICATION OF PAIN Based on source/ location/ referral & duration ACUTE PAIN / TRAUMATIC PAIN CHRONIC PAIN VISCERAL /SPLANCNIC PAIN SOMATIC PAIN MALIGNANT PAIN OR CANCER PAIN NON – MALIGNANT PAIN OR BENIGN PAIN SUPERFICIAL PAIN OR CUTANEOUS PAIN DEEP SOMATIC PAIN MUSCULOSKELETAL PAIN NEUROPATHIC PAIN

6. ACUTE PAIN Acute has a sudden onset, usually subsides quickly and is characterized by sharp, localized sensations with an identifiable cause Lasts > 30 days and occurs after muscle strains and tissue injury such as trauma or surgery and is described as a linear process A poorly treated pain can cause psychological stress and compromise the immune system due to the release of endogenous corticosteroids

7. Acute pain is usually characterized by increased autonomic nervous system activity resulting in Psychological symptoms such as anxiety Tachypnoea Tachycardia with hypertension Pallor Diaphoresis Pupil dilation

8. Visceral pain is a type of nociceptive pain that comes from the internal organs Unlike somatic pain it is harder to pinpoint Pain is described as general aching or squeezing pain It is caused by the activation of pain receptors in the chest, abdomen, or pelvic areas In cancer patients pain is caused by tumour infiltration, constipation, radiation & chemotherapy VISCERAL PAIN

9. SUPERFICIAL PAIN It is also known as cutaneous pain It arises from superficial structures such as skin & subcutaneous tissues It is a sharp, bright pain with a burning quality and may be abrupt or slow in onset DEEP SOMATIC PAIN It originates in deep body structures such as periosteum, muscles, tendons, joints & blood vessels Strong pressure, ischemia, tissue damage act as stimuli for brain damage Radiation of pain from original site of injury occur

10. CHRONIC PAIN C hronic pain is arbitrarily defined as pain lasting longer than 3 to 6 months It begins when pain persists after the initial injury has healed It is persistent or episodic pain of duration or intensity that adversely affects the function and well being of the patient It may be nociceptive, inflammatory, neuropathic or functional in origin It varies from unrelenting extremely severe pain to pain of escalating or non – escalating nature.

11. CHRONIC PAIN CYCLE

12. MAIN EFFECTS OF CHRONIC PAIN Effect on physical function Psychological changes Social consequences Societal consequences CONTRIBUTING BIOLOGICAL FACTORS Peripheral mechanisms Peripheral central mechanisms Central mechanisms

13. CHRONIC MALIGNANT PAIN It occurs in 60-90 % of patients with cancer Pain can be related to the tumour or cancer therapy or may be idiosyncratic Pain may also be found at the metastasized regions and treatment interventions may activate peripheral nociceptors Pain can be somatic/visceral CHRONIC NONCANCER PAIN It is also referred to as chronic non – malignant pain Pain may last for many years and is considered progressive in nature May be nociceptive, neuropathic or mixed in nature

14. NEUROPTHIC PAIN Neuropathic pain is a result of an injury or malfunction of the nervous system It is described as Aching Throbbing Burning Shooting Stinging Tenderness/ sensitivity of skin

15. MECHANISM OF NEUROPATHIC PAIN Nerve damage/ persistent stimulation Rewiring of pain circuits both anatomically & biochemically Spontaneous nerve stimulation Autonomic neuronal stimulation Increased discharge of dorsal horn neurons NEUROPATHIC PAIN Results in causing Finally leading to

16. MUSCULOSKELETAL PAIN This a type of chronic non cancer pain occurring due to musculoskeletal disorders such as Rheumatoid arthritis Osteoarthritis Fibromyalgia Peripheral neuropathies

17. BASED ON TRANSMISSION FAST PAIN Felt about 0.1 sec after a pain stimulus is applied It is described as sharp pain, pricking pain, acute & electric pain Fast sharp pain is not felt in most deeper tissues of the body SLOW PAIN Usually begins after 1 sec or more and may range from seconds to minutes Described as slow, burning, aching, throbbing, nauseous pain and chronic pain Associated with tissue destruction

18. OTHER TYPES OF PAIN REFERRED PAIN Pain that is perceived at the site different from its point of origin but innervated by the same spinal segment Usually applies to pain that originates from the viscera Eg. The pain associated with MI commonly is referred to the left arm, neck & chest BREAKTHROUGH PAIN Pain is intermittent, transitory & an increase in pain occurs at a greater intensity Usually lasts from minutes to hours and can interfere with functioning and QOL Eg. Neuropathic pain Lower back pain

19. PAIN RECEPTORS NOCICEPTORS or PAIN RECEPTORS are sensory receptors that are activated by noxious insults to peripheral tissues The receptive endings of the peripheral pain fibres are free nerve endings These receptive endings are widely distributed in the Skin Dental pulp Periosteum Meninges

20. SKIN RECEPTORS FOR PAIN HIGH THRESHOLD MECHANORECEPTORS ( HTMS) POLYMODAL RECEPTORS These receptors detect local deformation Eg: Touch These receptors detect a variety of stimuli causing injury Eg: Heat Noxious stimulation These do not have a specialized and simple nerve endings in the periphery

21. NERVE FIBRES INVOLVED IN PAIN TRANSMISSION A FIBRES C FIBRES A – BETA FIBRES A – DELTA FIBRES Large Myelinated Fast conducting Low stimulation threshold Respond to light touch Small Lightly Myelinated Slow conducting Respond to heat, pressure, cooling & chemicals sharp sensation of pain Small & unmyelinated Very slow conducting Respond to all types of noxious stimuli Transmit prolonged dull pain Require high intensity stimuli to trigger a response

22. PATHWAYS OF PAIN SENSATION The pathways of pain sensation are as follows Pathway from skin & deeper tissues Pathway from face – pain sensation is carried by trigeminal nerve Pathway from viscera – pain sensation from thoracic & abdominal viscera are transmitted by sympathetic nerves & from oesophagus, trachea & pharynx by glossopharyngeal nerves Pathway from pelvic region – conveyed by sacral parasympathetic nerves

23. PATHWAY FROM SKIN & DEEPER TISSUES

24. PAIN PATHWAYS ASCENDING PAIN PATHWAY

25. DESCENDING INHIBITORY PAIN PATHWAY

26. ENDOGENOUS ANALGESIC MECHANISMS The endogenous analgesic mechanism comprises of endogenously synthesized opioid peptides, which are MORPHINE like substances The opioid like substances are found at different points of the brain which are breakdown products of 3 large protein molecules Pro – opiomelanocortin: β – endorphin Pro – encephalin: Met – encephalin & Leu – encephalin Prodynorphins: Dynorphins These are found in peripheral processes of 1 afferent neurons, human synovia, many regions of CNS

27. MECHANISMS OF PAIN Pain sensation involves a series of complex interactions between peripheral nerves & CNS Pain sensation is modulated by excitatory and inhibitory NTs released in response to stimuli Sensation of pain is composed of 4 basic processes Transduction Transmission Modulation Perception

28. PAIN THEORIES Pain theories are proposed to offer the possible physiologic mechanisms involved in pain. They are as follows Specificity theory Pattern theory Neuromatrix theory Gate control theory SPECIFICITY THEORY: This theory states pain as separate modality evoked by specific receptors that transmit information to pain centres or regions in the forebrain where pain is experienced.

29. PATTERN THEORY Pain receptors share endings or pathways with other sensory modalities but different patterns of activity of the same neurons can be used to signal painful and non – painful stimuli Eg. Light touch applied to skin would produce the sensation of touch and intense pain pressure would produce pain through high frequency firing of the same receptor NEUROMATRIX THEORY This theory was put forward by MELZACK This theory explains the role of brain in pain as well as the multiple dimensions and determinants of pain

30. Acc to this theory the brain contains a widely distributed neural network called the body self Neuromatrix that contains somatosensory, limbic, & Thalamocortical components The body self Neuromatrix involves multiple input sources such as Somatosensory inputs Other impulses/ inputs affecting the interpretation of the situation Various components of stress regulation systems Intrinsic neural inhibitory modulatory circuits

31. GATE CONTROL MECHANISM Proposed by MELZACK & WALL IN 1965 According to this theory, the pain stimuli transmitted by afferent pain fibres are blocked by GATE MECHANISM located at the posterior gray horn of the spinal cord If the gate is open pain is felt , and if the gate is closed pain is suppressed Impulses in A – δ & C – fibres can be blocked by modulated by A – β activity that can selectively block impulses from being transmitted to the transmission cells in the spinal cord and then to CNS resulting in no pain

32. ROLE OF BRAIN IN GATE CONTROL MECHANISM Gates in spinal cord are open Pain signals reach the thalamus through lateral spinothalamic tract Signals are processed in thalamus Signal are sent to sensory cortex & perception of pain occurs in cortex Signals are sent from cortex back to spinal cord and the gate is closed by releasing pain relievers such as opioid peptides Minimizing the severity & extent of pain

33. ASSESSMENT OF PAIN METHOD OF PAIN ASSESSMENT Comprehensive history intake Medical history Physical history Family history Physical exam Questioning on characteristic of pain – onset, duration, location, quality, severity & intensity Evaluation of psychological status

34. PAIN ASSESSMENT PNUEMONIC P – Palliative/ P rovocative/ Precipitating Q – Quality R – Radiation/ Region S – Severity T – Temporal/ Time related The impact of pain on the patients functional status, behaviour and psychological status should also be assessed

35. PAIN ASSESSMENT TOOLS Pain may be accompanied by physiologic signs and symptoms and there are no reliable objective markers of pain The severity of pain can be assessed by rating scales & multidimensional scales . RATING SCALES Provide a simple way to classify the intensity of pain and should be selected based on the patients ability to communicate MULTIDIMENSIONAL SCALES H elpful in obtaining information about the pain and impact on QOL, but are more often time consuming to complete

36. RATING SCALES SIMPLE DESCRIPTIVE PAIN INTENSITY SCALE NO PAIN MILD PAIN MODERATE PAIN SEVERE PAIN VERY SEVERE PAIN WORST POSSIBLE PAIN NUMERIC SCALE

37. VISUAL ANALOG SCALE (VAS) FACES SCALE

38. VERBAL RATING SCALE PAIN THERMOMETER

39. MULTIDIMENSIONAL ASSESSMENT SCALES The following are the types of MAS Initial pain assessment tools Brief pain inventory McGill pain questionnaire The neuropathic pain scale The Oswestry disability index

40. DIAGNOSIS OF CHRONIC PAIN

41. CLINICAL PRESENTATION OF PAIN General: Acute distress/ trauma pain No noticeable suffering (Chronic pain ) Symptoms: Sharp, dull, burning, shock like, tingling, shooting radiating, fluctuating in intensity and varying in location N on – specific: Anxiety Depression Fatigue Insomnia Anger and fear

42. SIGNS OF PAIN ACUTE PAIN Hypertension Tachycardia Diaphoresis Mydriasis Pallor CHRONIC PAIN There may be no obvious pain signs in some acute cases and in most chronic/ persistent pain LABORATORY TESTS Pain is always subjective i.e. there are no laboratory tests It is diagnosed based on patients description and history

43. MANAGEMENT OF PAIN GOALS OF THERAPY To decrease the subjective intensity To reduce the duration of the pain complaints To decrease the potential for conversion of acute pain to chronic persistent pain syndromes To decrease the physiological, psychological, & socioeconomic sequelae associated with under treatment of pain To minimize ADRs, & Dis intolerance to pain management therapies Improving the patients QOL and the ability to perform activities of daily living

44. APPROACHES TO PAIN CONTROL

45. NON – PHARMACOLOGICAL MANAGEMENT The non – pharmacological management involves the following approaches Physiotherapy Psychological techniques Stimulation therapies – Acupuncture & Transcutaneous Electrical Nerve Stimulation (TENS) Palliative care – involves the alleviation of symptoms but does not cure the disease

46. SURGICAL PROCEDURE FOR THE RELIEF OF PAIN CORDOTOMY: In the thoracic region , the spinal cord opposite to the side of pain is partially cut to interrupt the anterolateral pathway THALAMOTOMY: Involves causter ization of specific pain areas in the intrathalamic nuclei in the thalamus, which often relieves suffering type of pain

47. SYMPATHECTOMY Excision of the segment of the sympathetic nerve or one or more sympathetic ganglia RHIZOTOMY Surgical removal of spinal nerve roots for the relief of pain or spastic paralysis

48. FRONTAL LOBOTOMY Surgical process involving division of one or more nerve tracts in a lobe of the cerebrum usually frontal lobe

49. PHARMACOLOGICAL MANAGEMENT

50. OPIOID/ NARCOTIC ANALGESICS OPIUM is a raw extract of the poppy plant Papaver somniferum During 19 th century, MORPHINE was isolated from opium and its pharmacological effects were characterized OPIOD RECEPTORS TYPE CHARACTERIZATION µ - MU Highly selective for opioids δ – DELTA Mixed agonist – antagonist response K - KAPPA Opioid analgesics selective for these receptors are not identified

51. LOCATION OF OPIOID RECPTORS

52. OPIOID CLASSIFICATION

53. MECHANISM OF ACTION OF OIPOIDS

54. MAJOR PHARMACOLOGICAL EFFECTS OF OPIOIDS ORGAN SYSTEM EFFECTS CENTRAL NERVOUS SYSTEM Analgesia Dysphoria Miosis Physical dependence Respiratory depression Sedation CARDIOVASCULAR SYSTEM Decreased myocardial O 2 demand Vasodilation Hypotension GASTROINTESTINAL SYSTEM Constipation Nausea & Vomiting GENTIOURINARY SYSTEM Increased bladder sphincter tone Urinary retention

55. ORGAN SYSTEM EFFECTS NEUROENDOCRINE EFFECTS Inhibition of release of leutinizing hormone (LH) Stimulation of release of ADH & Prolactin IMMUNE SYSTEM EFFECTS Suppression of function of natural killer cells (NK cells) DERMAL EFFECTS Flushing Pruritus Urticaria

56. OPIOID ANALGESIC THERAPY IN PAIN

57. MANAGEMENT OF OPIOID ADVERSE EFFECTS ADVERSE EFFECT MANAGEMENT EXCESSIVE SEDATION Reduce dose by 25% or increase the dosing interval CONSTIPATION CASANTHROL – DOCUSATE 1 capsule at bed time/ BD SENNA 1 – 2 tablets at bed time/ BD BISACODYL 5 – 10mg daily + DOCUSATE 100mg BD NAUSEA & VOMITINGS HYDROXYZINE 25 – 100mg (PO/IM) every 4 – 6 hrs as needed DIPEHNHYDRAMINE 25 – 50mg (PO/IM) every 6 hours as needed ONDANSETRON 4mg IV or 16mg PO, 4 – 8mg IV every 8 hours as needed PROCHLORPERAZINE 5 – 10mg (PO/IM) every 3 – 4 hrs, 25mg/ rectum BD

58. ADVERSE EFFECT MANAGEMENT GASTROPARESIS METOCLOPRAMIDE 10mg (PO/IV) every 6 – 8 hours VERTIGO MECLIZINE 12.5 – 25mg PO every 6 hours URTICARIA/ ITCHING HYROXYZINE 25 – 100mg (PO/IM) every 6 hours as needed DIPHENHYDDRAMINE 25 – 50mg (PO/IM) every 6 hours as needed RESPIRATORY DEPRESSION MILD: Reduce dose by 25% MODERATE – SEVERE: NALOXONE 0.4 – 2mg IV every 2 – 3 minutes (up to 10mg) 0.1 – 0.2mg IV every 2 – 3 minutes until desired reversal CNS IRRITABILITY Discontinue OPIOID, treat with BENZODIAZEPINES

59. INERTACTING DRUGS EFFECT OPIOIDS + CNS DEPRESSANTS Eg: ALCOHOL ANESTHETICS ANTIDEPRESSANTS ANTIHISTAMINES BARBITURATES BENZODIAZEPINES PHENOTHIAZINES Additive CNS depressant effects MEPERIDINE + MAO – I Result in severe reactions such as Excitation, sweating, rigidity, and hypertension DRUG INTERACTIONS

60. NON OPIOID ANALGESICS Nonsteroidal Anti-inflammatory Drugs (NSAIDS) are usually considered as Non Opioid Analgesics CHARACTERISTICS FEATURES: Relieve pain without interacting with opioid receptors Possess anti – inflammatory properties Have antiplatelet activities Do not cause sedation & sleep Are not addicting

61. MECHANISM OF ACTION OF NSAIDS

62. MECHANISM OF ACTION OF COX – 2 INHIBITORS

63. NON – OPIOID ANALGESIC THERAPY

64. ADVERSE EFFECTS OF NON NARCOTIC ANALGESICS ORGAN SYSTEM EFFECTS GASTROINTESTINAL Nausea Abdominal pain Dyspepsia Constipation Vomiting Haematochezia Intestinal obduction Intestinal perforation Pancreatitis Peritonitis PUD Diarrhoea HEMATOLOGICAL Aplastic anaemia Leukopenia Neutropenia Pancytopenia Thrombocytopenia MALIGNANCIES Lymphomas

65. ORGAN SYSTEM EFFECTS RENAL EFFECTS Interstitial nephritis Impaired renin secretion Enhanced tubular water/ Na + reabsorption INFECTIONS Sepsis leading death MALIGNANCIES & INFECTIONS ARE AS A RESULT OF TNF -  INHIBITORS INTERACTING DRUGS EFFECT ASPIRIN – ORAL ANTICOAGULANTS Gastric mucosal bleeding, & increased risk of bleeding SALYCYLATES - METHOTREXATE Blockage of METHOTREXATE tubular secretion by SALICYLATES resulting in pancytopenia or hepatotoxicity due to increased METHOTREXATE NSAIDS – TNF BLOCKING AGENTS Neutropenia

66. WHO ANALGESIC PAIN LADDER

67. ALGORITHM FOR ACUTE PAIN MANAGEMENT

68. ALGORITHM FOR CHRONIC CANCER PAIN MANAGEMENT

69. THANK U