Facial pain non odontogenic causes-part1

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  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM
  • 08/13/12 12:55 PM 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
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM Expand on neural plasticity here – changes in chronic pain vs acute pain is important
  • 08/13/12 12:55 PM 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
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM Pain signals in the form of electrical impulses are carried by peripheral nerves called nociceptors (C-fibers) that synapse with neurons in the dorsal horn of the spinal cord. The pain signal is then transmitted via the spinothalamic tract to the cerebral cortex, where it is perceived, localized, and interpreted. The body’s pain-relieving, or antinociceptive, system balances out the pain-sensing system. When pain signals transmitted by peripheral nerves, or nociceptors , arrive in the brain, they activate neurons in the periaqueductal gray matter of the brain and the nucleus raphe magnus of the brainstem, which release endorphins and enkephalins. In addition to pain signals, other stimuli can trigger activation of the anti-nociceptive system, such as exercise, meditation, and comforting or reassurance. This explains the utility of many of the behavioral components of pain management programs. Image adapted with permission: Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35(7): 45-52, 59. ©The McGraw-Hill Companies, Inc. Illustration by Seward Hung. Besson, JM. The neurobiology of pain. Lancet. 1999;353:1610-1615 .
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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.
  • 08/13/12 12:55 PM 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 .
  • 08/13/12 12:55 PM
  • 08/13/12 12:55 PM 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.
  • Facial pain non odontogenic causes-part1

    1. 1. FACIAL PAIN-NON ODONTOGENIC CAUSES Prof. A.V. SRINIVASAN, MD, DM, Ph.D, D.Sc(hon)F.A.A.N, F.I.A.N. Emeritus Professor The Tamilnadu Dr. M.G.R. Medical University Former Head Institute of Neurology, Madras Medical College Ragas dental college-7-09-11
    2. 2. Facial Pain Understanding, Impact and AwarenessWe learn by thinking and the quality of the learning outcome is determined by the quality of our thoughts R.B. Schmeck
    3. 3. “Pain May be Inevitable, but Misery is Optional” Dee MalchowPain 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
    4. 4. Pain is undertreated 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.
    5. 5. Indian Scenario 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
    6. 6. Decade of Pain Control and Research In late 2000, US Congress passed into law a provision, which the president signed , that declared the 10 year period beginning Jan 1st 2001, as the Decade of Pain Control and Research. The American Pain Society has actively supported 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.
    7. 7. What is Pain?• 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 The International Association for the• Pain is a significant stress physically, emotionally pain an Safety of Pain (IASP) defines 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)
    8. 8.  Qualities of Pain Organic vs. psychogenic Acute vs. chronic Malignant or benign Continuous or episodicPerceiving 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
    9. 9. Acute vs. Chronic Pain ACUTE CHRONICFunction To warn None (destructive)Etiology Usually Clear Complex/obscurePt. Mood Anxiety/fear Depression/angerMD impact Comforting Frustrating/drainingRole of Rx Control/cure Improve function/QOL
    10. 10. Categorization of Chronic pain 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 CentralSuperficical / /SomaticSuperficical 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, NewJersey: Humana Press. p. 304
    11. 11. Different types of painNociceptive descriptors Neuropathic descriptors Cramping, tender Shooting Gnawing, heavy Hot-burning Aching Sharp Splitting Stabbing
    12. 12. Multidimensional Classification of PainIASP (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: 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 et al, 2001; Merskey et al, 1994)
    13. 13. Dimensions of Chronic Pain Chronic pain has a psycho- Depressio Hostil social component that must ity be dealt with before n depression becomes a part of Psychological Loneline the clinical picture. Chronic Pathological Anxie pain should be recognized as Factors Physical Process Social Factors Factors a multi-factorial disease state ss ty requiring intervention at many levels.A.G. Lipman, Cancer Nursing, 2:39, 1980 TIME
    14. 14. Pain: Social and Psychological Factors  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 managementGive us the GR ACE to acce pt with se re nity the thing s that canno t bechang e d the COURAGE to chang e the thing s that sho uld be chang e d and the WISDOM to kno w the diffe re nce
    15. 15. Current Understanding of Pain  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. 98) 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
    16. 16. Understanding Pain Pathophysiology
    17. 17. What causes pain?  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)
    18. 18. Peripheral and Central Pathways for Pain Ascending Tracts Descending Tracts Cortex Thalamus Midbrain Pons Medulla(Brookoff, 2000) Spinal Cord
    19. 19. Pain Pathway
    20. 20. Nerve Fibres 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
    21. 21. Pathophysiology of Chronic Pain In chronic pain, the nervous system remodels continuously in response to repeated pain signals – nerves become hypersensitive to pain – nerves 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)
    22. 22. Pain-Sensing System in the Malfunction in Chronic Pain Acute pain: Pain Pain-sensing signals Sensing are initiated in response to a stimulusIn chronic • They elicit a pain-pain, pain relieving responsesignals aregenerated Chronic pain:withoutphysiologic Pain signals aresignificance generated for no reason and may be intensified • Pain-relieving (Illustration: Seward Hung, 2000) mechanisms may be defective or deactivated
    23. 23. Role of Serotonin and Norepinephrine 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
    24. 24. Pathophysiology of Pain Inferred from characteristics, etiology or pathophysiology Types – Nociceptive – Neuropathic – Idiopathic Therapeutic implications(Portenoy et al, 1996)
    25. 25. Nociceptive Pain 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 afferent neurons – Visceral: related to activation of visceral afferent neurons(Loeser et al, 2001; Portenoy et al, 1996)
    26. 26. Neuropathic Pain 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”  deafferentation pain (central pain, phantom pain)  Sympathetically-maintained pain – Presumed “peripheral generator”  Polyneuropathies and mononeuropathies(Portenoy et al, 1996)
    27. 27. Idiopathic and Psychogenic Pain 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)
    28. 28. Recent Developments In Pain Management  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)
    29. 29. Progress in Chronic Pain Management: Therapeutic Modalities for Chronic Pain Management Assessment
    30. 30. “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
    31. 31. Pain Assessment  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)
    32. 32. Pain Assessment 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)
    33. 33. Pain Intensity Rating Scales• 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)
    34. 34. Progress in Chronic Pain ManagementTherapeutic Modalities for Chronic Pain Management Treatment
    35. 35. Therapeutic Options for Chronic Pain Management Pharmacotherapy (Analgesics)  Non-opioids  Adjuvant Analgesics  Antidepressants  Anticonvulsants  Opioids Rehabilitative Approaches Psychologic Interventions Anesthesiological Approaches Neurostimulatory Techniques Surgery Complementary/Alternative Approaches Lifestyle Changes (Cashman, 1996; Portenoy et al, 1997; Hanks et al, 1998; Galer, 1998; Stein, 1995)
    36. 36. Status of antidepressants in chronic pain management 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 effectsNeurologic 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)
    37. 37. INTRODUCTION  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
    38. 38. PATHOPHYSIOLOGY  Pain  Referred pain – Pattern of referred painSuccess in life is a matter not so much of talent and opportunity as of concentration and perseverance - C.W. Wendte
    39. 39. CLINICAL ASSESSMENT  History – Hx of present illness – Past medical hx – Family hx – Social hx  Physical examinationWe 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
    40. 40. CLINICAL ASSESSMENT  Clinical features suggesting serious cause – Crescendo – Early morning – Vomiting – Fever – Seizures & other neurological symptomes – Worst headache in my life – Known malignancy – Tenderness
    41. 41. Facial painTypical Neuralgias1) Trigeminal neuralgia • Characterized by recurring paroxysmal severe pain, brief duration (seconds) in the territory of the trigeminal nerve, spontaneously or initiated by chewing, talking, touching the affected side of the face. • Unknown aetiology, an arterial loop pushing on the sensory root in the posterior fossa. • Females affected more than males • Analgesics, surgery, destruction of the sensory neuron, division of nerve root.
    42. 42. Facial painTypical Neuralgias2) Glossopharyngeal 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
    43. 43. Facial painTypical Neuralgias3) 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 nerve. • Analgesics, vidian neurectomy
    44. 44. Facial pain Posttraumatic neuralgia – Neuroma – Parietal & occipital – 90% recovery Experience can be defined as yesterday’s answer to today’s problems
    45. 45. Facial PainAtypical 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
    46. 46. Symptomatic NeuralgiasIntracranial lesions1) Central lesions • Tumours of the brain stem, M.S., thrombotic lesions, metastasis, occult naso-pharyngeal ca. • No precipitant, sensory loss.2) Post herpetic neuralgia • Herpes zoster may affect trigeminal nerve ganglion • Vesicular rash covers one division commonly the 1st with severe pain.
    47. 47. Symptomatic NeuralgiasExtracranial lesions1) Sinus disease • Infective and neoplastic lesions of the paranasal sinus. • Facial pain & dental pain, loss teeth. • Clinical suspicion. • Treatment2) Dental neuralgia • Dental carries • Dental extraction3) Temporomandibular joint pain
    48. 48. HeadacheHeadache is one of the commonest symptoms in medical practice.Aetiology:1) Raised intracranial pressure 
    49. 49. Headache3) Migraine  Congenital predisposition  Triggered by hunger, certain foods, sleep - too much or too little, hormonal variations, stress.  Pathology-vascular dilatation  Females affected more than males  ? Proceeded by aura usually visual, paraesthesiae of hands, weakness  Headache is unilateral or bilateral, affects any area of the head, aching or throbbing often accompanied by nausea and vomiting  Diagnosis - by history alone  Treatment - prevention by avoiding precipitating factors, appropriate medication.
    50. 50. Headache4) Tension headache  More common in adult females  Positive family history (40%)  Maybe associated with migraine  Produced by persistent contraction of the muscles of the neck, head and face  Caused by emotional tension, secondary to other headaches, posture habit  Treated by analgesics, muscle relaxants, physiotherapy
    51. 51. Headache5) 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
    52. 52. Pains from head and neck musclesPain 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.
    53. 53. Pains from head and neck musclesPain from upper neck muscles  Can radiate over the head Treatment by physio-therapist or rheumatologistPain from frontalis muscles  Usually due to bad posture at work or while driving Treatment: physio-therapy
    54. 54. Pains from head and neck musclesCervical spondylosis  Pain mediates upwards from the neck to the occiput or vertex to the front of the head, down to the shoulders  Due to cervical discs prolapse  Diagnosis - x-ray Treatment: Physio-therapy, referral to rheumatologist
    55. 55. Pains from head and neck musclesTemporal arteritis  Due to acute inflammation of the artery, the cause unknown, affects 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, partial or complete loss of vision.  ESR Elevated Treatment: Cortisone, analgesics
    56. 56. Pains from head and neck muscles Psychologic headache  Usually accompanied by depression, anxiety  No organic lesionIt is a great misfortune not to possess sufficient wit to speak well nor sufficient judgment to keep silent La Broyers character
    57. 57. Dedicated to my family formaking everything worthwhile
    58. 58. Thank you
    59. 59. READ not to contradict or confute Nor to Believe and Take for Granted but TO WEIGH AND CONSIDERTHANKYOU My sincere thanks to P.Sampath
    60. 60. Cerebrovascular Emergencies Is survival a mere stroke of Luck?“My Opinions are founded on knowledge but modified by experience”
    61. 61. Every minute matters: ‘time is brain’ Expert is one who think to his chosen mode of ignorance
    62. 62. INTRODUCTION Perceptual Sense (Observation) Word Sense (Recording) Common Sense (Thinking) – Will lead you to get - Clinical Sense “ He who cannot forgive others destroys the bridge over which he himself must pass” - Annoy
    63. 63. Cerebrovascular disease – Mind boggling facts World wide incidence: 2/1000 population/annum 1 Incidence in people aged 45 – 84 years: about 4/1000 1 Incidence in India: was 36/100,000 for the year 1998-1999 3 in a study in Calcutta Incidence of mortality due to stroke (India: WHO study): 73/100,000 per year2CVD is the most disabling of all neurologic diseases.50% of survivors have a residual neurologic deficit. Greater than 25% require chronic care. 1.A practical approach to management of stroke patients; 1996; 360-384 2. Epidemology of cerebrovascular disorders in India; 1999; 4-19 3. Neuroepidemiology 2001;20:201-207 If you think you can or you can’t You are always right
    64. 64. Annual risk CVD, MI, vascular death following TIA, minor CVD• CVD 6.7 %• MI 2.5 %• Death 7.2 %• CVD, MI, Vascular death 8.6 %• CVD, MI, Death 10.3 % Experience can be defined as yesterday’s answer to today’s problems
    65. 65. Indian scenario 1880 death / day due to stroke in IndiaEqual to 6 Boeings 737 crashes every day
    66. 66. Indian scenario Number of deaths due to stroke 22 times that due to malaria 4 times that due to RHD 1.4 times that due to TB Almost equal to deaths due to IHD
    67. 67. Comparison India vs. established market economies (Age adjusted stroke mortality) 2 to 3 times stroke mortality higher in India Indian immigrants to England have higher risk or dying due to stroke than local population
    68. 68. ComparisonUSA – stroke mortality decline since 1940’sIndia likely to increase– Increase life expectancy (aging population)– Urbanization
    69. 69. Acute stroke interventions – reasonable evidence Stroke units Aspirin Thrombolysis Heparin
    70. 70. Stroke Vascular event due to atherosclerosis Relevant to all of us Neurologists Cardiologists Physicians
    71. 71. Stroke disability worldwide  Limb weakness – 77%  Urinary disturbance – 48%  Dysphagia – 45%  Cognitive deficit – 44%35% functionally dependent at 1 year
    72. 72. Acute stroke interventions – evidence based medicine Stroke care units vs general wards – 9% relative risk reduction – 56 deaths or dependency avoided / 1000 acute strokes treated / year Aspirin – 3% relative risk reduction – 12 deaths or dependency avoided / 1000 active strokes treated / year
    73. 73. Acute stroke interventions – evidence based medicine Thrombolysis – (even in USA only 1% of strokes are thrombolysed) – 10% relative risk reduction – 63 deaths or dependency avoided (91 early deaths due to haemorrhage) Heparin – No benefit
    74. 74. Conclusion People who survive stroke – 90% are left with deficit – minimal / mild / moderate / severe None of the presently available therapy has any major impact hence prevention is critical
    75. 75. New role of doctors“Managers of Change”“Preventors of Change”(Health ill health)
    76. 76. Global 15 million deaths globallyevery year due to vascular disease (30% of all deaths)
    77. 77. Global By 2020 – stroke and myocardialinfarction will constitute leading cause of death / disability
    78. 78. Lowering blood pressure Primary prevention – 17 randomised trials – reduction of 5 to 6 mmHg diastolic and 10.12 mmHg systolic BP – 38% reduction of stroke Secondary prevention – have we made PROGRESS
    79. 79. Common Stroke Mimics Hypoglycemia Post ictal state Drug overdose Concussion with neck injury Migrainous accompaniment Encephalopathies with focal signs Hyponatremia Subdural hematoma, Empyema Focal Encephalitis: Herpes Being ignorant is not so much a shame as being unwilling to learn
    80. 80. Guidelines for 24 hrs – MandatoryLevel of EvidenceLevel A: Based on RCT or Meta analysis of RCTLevel B: Based on Robust Experiment or Observation StudiesLevel C: Based on Expert opinion.“The True Art of Memory is The Art of Attention” - S.Johnson
    81. 81. 1. History And Examination a. Stroke clerking Performa (1994) R.C.P. 1. Improved patient Assessment 2. Improved Management - not clear 3. Improved outcome - not clear b. Examination 1. Secure Diag of Stroke 2. Specify Impairment 3. Identify sub type of Ischemic stroke 4. Rule out stroke mimics “ We Sometimes think we have forgotten something when in fact we never really learned it in the first place” Imp.Your Memory Skills
    82. 82.  Guideline: 3 (B) - CPR – CPR is rarely successful in the setting of stroke – Sneeder 1993. Guideline: 4(B) Investigations:(Sagar 1995)- 435 PTS) – Chest x-ray 16% ABN – Only 4% change clinical management – Order x-ray chest if weight loss or chest symptoms presentThrough Action You Create your Own Education - D.B. ELLIS
    83. 83.  Guideline 5: (B) ECG: – Cardiac cause of Death (30 days) Ebrahim 1990. – All conscious patients to have ECG Guideline 6: (C) CT: – Routine CT Head is a must – King’s fund forum(1988) gives useful framework – Weir 1994 Clinical scoring cannot distinguish – CT done if: a) Uncertainty of Stroke b) If Anticoagulation or Anti Platelet treatment contemplated c) IV rtPA Thought is the labour of the intellect Reverie is its pleasure
    84. 84.  Guideline 7:(B) M.R.I. – Mohr 1995, - Unclear for Implications for clinical practice – 2004 – PWI > DWI – IV rtPA very useful Whatever the Mind can conceive and Believe, the mind can Achieve -Napoleon Hill
    85. 85.  Guideline 8: (B) ECHO no Routine– Echo in Acute Stroke – Cardiac cause/Thrombus LV– TEE is superior to TTE– Amer Heart Asson (1997) - same conclusion– Yield is very low. (Leung 1993; Chambors 1997)– Only when abnormal ECGS - change clinical management Imagination is more Important than Knowledge
    86. 86.  Guideline 9: (A) – Doppler scan for selected patients – > 80% stenosis benefits from Endarterectomy – Subst Storke -Good recovery - do doppler – Useful in posterior circulation A open foe may prove a curse ; but a pretended friend is worse
    87. 87.  Guideline 10: (B) Management: – Fever (Worst Prog.) Reith 1996 – Hypoxia (Moroney 1996) - Exac. by seizures Pneumonia and Arrythmias - Worst outcome – Hyperbaric O2 ineffective (Nighoghossaln 1995) – Haemodilut. Plasm Expanders; venesection – No evidence for efficacy (As plund - 1997) Check ABG only if Hypoxia suspected. It is a great misfortune not to possess sufficient wit to speak well nor sufficient judgment to keep silent - La Broyers character
    88. 88.  Guideline 11: (A) Steroids and Hyperosmolar agents Unproven treatment – – Tumor oedma responds but not cytotoxic stroke oedma qialbash 1997 - No effect on survival or improv. In funct. Outcome – Mannitol - (Boysen 1997) - short term effective statistically in conclusive You are what you think and not what you think you are
    89. 89.  Guideline 12: (B) - Blood Pressure – Defer - acute reduction of BP - 10 days unless HT Encephalopathy or aortic dissection present – Moris 1997 - Increase BP - falls in 10 days – UK - 5mm in D.B.P. 1/3 storke - Low BP prompt correct of hypovoll. and withdrawal of hypotonic drugs – Collins 1994 - HT - Prim. stroke prevent – Neal 1996 (Current RCT) - HTs in stroke survivors -study needed – Acute reduction of BP only if thrombolysis considered We learn by thinking and the quality of the learning outcome is determined by the quality of our thoughts R.B. Schmeck
    90. 90.  Guideline 13: (A/B) – AF – AF / ISCH Stroke/ Mild disability - Warfarin after 48 Hrs (Longer for larger) – Aspirin for others EAFT 1995 Less than 2 PT - No effect SPAF 1996 > 5 - BleedingDiscipline Weighs ounces; Regret weighs Tons
    91. 91.  Guideline 14:(B/C) - Blood sugar – Weir (1997) > 8 mm d/Lit - Poor outcome – Acute MI + 11 mm d/Lit - Intensive Insulin - improved (Malmberg 1997)A great many people think they are thinking when they are merely re arranging their prejudices W. James
    92. 92.  Guideline 15: (A) Cholesterol – Prosp. Study collob.: 1993 - Epidem study do not support – Blaun 1997: Metranauetic - Chollest & statin 30% decrease - stroke in CAHD patients. – Sacks 1996 - Tot chol: decrease to 4.8 mmol/Lit benefitsMany Ideas grow better when transplanted into another mind than in the one where they sprang UP O.W. Holmos
    93. 93.  Guideline 16: (A/C) Deep vein thrombosis – Kalra 1995 - 10 days - stroke Pts - 50% – Sandercock 1993 - Pul embol 6-16% only – Ist 1997 - 5000 IV or 12500 twice daily - Hemorrage greater – Gradual stocking value - useful in Surg - pts but its value not evaluated - (Wells 1994) – Use with caution - if periph artery insuf. is present hence do not use heparin on stockings. A woman’s desire for revenge outlasts all her other emotions
    94. 94.  Guideline 17: (A/B) Pressure sure – Event health care (1995) specialised low pressure mattress systems to be used than stand Hospital - mattress Every discovery contains an irrational element or 4 creative intuition
    95. 95.  Management of infarction – Guideline 18: (A)  Aspirin 75 - 150 /Day  3 yrs 40% reduces of vascular events in 1000 pts (APTC - 1994)  Stroke sub type value ? (TACI, PACI, LACI, POCI)  Dienners - 1996, synergy possible with Clopidogrel Ticlopidine etc.I have never let my Medical schooling interfere with my education Mark Twain
    96. 96. Anti Coagulation Warfarin - AF – In sinus rhythm - uncertain – Spirit 1997 low dose ABP + Warfarin in TIA & Minor stroke - Stopped of HE – Heparin (IST 1997) – Significant reduction in early death (12 fewer in 1000) not better than aspirin – So avoid Heparin (A) “ H who cannot forgive others destroys the e bridge over which he himself must pass” -
    97. 97.  Thrombolysis (A)  Warlow 1997 - Uncertain clinical benefit  2004 – NINDS – Thrombolysis conclusively proved its efficacy – first 3 hrsWhen they tell you to grow up, they mean stop growing Piccaso
    98. 98.  Guideline 20: (I) Hemorrhage – Hankey and hon 1997: Supra tentorial evacuation for ICH is controversial - Avoid – Infra tentorial - Yes – Main Indication - Deteriorating or depressed consciousnessA (Neurologist’s) life is like a piece of paper on which everyone who passes by leaves an impression - Chines proverb
    99. 99. 2 2 4 P ts Guideline 21 : Ventilation 131 I n t u b a tio n 93 N o t In tu b -Decreased level of consciousness - increased 6 4 D is c h a r 6 7 D ie d mortality and poor final3 4 R e d ta g 2 1 d is c h t o n ver h om e 8 D is c fo r p a llim a 1 D is c H om e outcome - Absent pupillary light 3 D ie d 7 D ie d 3 D ie d responses - poor prognosisA medical school should not be a preparation for life. A school should be life
    100. 100. PITFALLS Basing treatment of stoke on brain imaging along without a vascular work-up Missing early infarct signs on CT Underestimating the time of symptom onset for patients who wake up with a stoke Overtreatment of hypertension in acute stokeThree can be seen in the divisions of a human in mind, body and spirit
    101. 101. PITFALLS Overuse of carotid endarterectomy in asymptomatic patients Not investigating both extracranial and intracranial circulations Failure to distinguish severe cartid stenosis from total occlusion Not obtaining spinal fluid for patients with suspected subarachnoid hemorrhage “Social Isolation is in itself a pathogenic Factor for disease production”
    102. 102. PITFALLS Not treating patients with large artery ischmic stroke indefinitely with antiplatelet terapy Failure to recognize lacunar stoke Inadequate use and dosing ofHMG Co-A reductase inhibitors (statins) inpatients with cerebrovascular disease Through Action You Create your Own Education - D.B. ELLIS
    103. 103. PROGNOSTIC PEARLS Flaccid Paralysis for more than 96 hrs When tendon reflexes recover without return of voluntary movement – prognosis poor Recovery of sensory less in usual to a degree. Postion sense recovers but not pain and temperature Recovery from Dysphasia is never complete Dysarthria usual improves and Dysphagia never improves Diplopia due to brain stem is usually permanent Conjugate gaze – recovers Vertigo improves but hearing loss is permanent Pseudobulbar palsy permanent “ByNature All Men/W en are alike but om byEducation widelydifferent”
    104. 104. STOKE MYTHOLOGY GENERAL MYTHS DIAGNOSTIC MYTHS THERAPEUTIC MYTHS Serious, sincere, systematic study surely secures supreme success
    105. 105. GENERAL MYTHS PHYSICIAN+ MRI = NEUROLOGIST MINISTROKE CHAOTIC CVA COMMUNICATION Discipline Weighs ounces Regret weighs Tons
    106. 106. DIAGNOSTIC MYTHS Self evident cause Ischaemic stroke + AF Lacunes, Lacunar infarcts and small vessel disease Cryptogenic stroke PFO and Cardiogenic stroke Experience can be defined as yesterday’s answer to today’s problems
    107. 107. Ultrasound DiagnosisIn skilled hands, ultrasound may show:• Carotid occlusion or stenosis• MCA occlusion or stenosis• Vertebrobasilar occlusion• Extracranial dissection The secret of walking on water is Knowing where the stones are
    108. 108. UCLA Stroke CT ProtocolsSequence Time CT CT CT CT CT Stroke Stroke Stroke reduced WWO Stroke WWO reduced Dye Diamox Dye WWO Diamox SCOUT 0’15” + + + + + CT 0’30” + + + + +CTA-COW - + + + + 16’CTA-Neck - + + + + CTP 20’ - + + + + CTP W 30’ - - + - + diamox Post- 0’30” + - - - -contrast
    109. 109. Magnetic Resonance Imaging (MRI)1 High level of anatomic detail for precisely locating the stroke and determining the extent of damage. Especially useful for small blood vessels due to high sensitivity Advances in the early detection of stroke involve using diffusion and perfusion weighted imaging. 1. Curr Opin Neurol. 2004 Aug;17(4):447-51 Memory, the daughter of attention, is the teeming mother of knowledge - Martin Tupper
    110. 110. UCLA Stroke MRI ProtocolsSequence Time Brain TIA Stroke Thrombol Thrombol WWO ysis 1 ysis 2 SCOUT 0’25” + + + + +MRA-Neck 6’44” - + + - + DWI 0’40” - + + + + T2 3’42” + + + + +MRA-COW 6’12” - + + + - FLAIR 2’41” + - + + - GRE 2’35” - - + + + PWI 2’ - - - + + T1 3’ + - - - - T1 post 3’ + - - - - Gad
    111. 111. Other Diagnostic Tools-1Magnetic Resonance Angiography1 (MRA)Carotid Duplex Scanning2:Transcranial Doppler (TCD)3Xenon CT Scanning4 Science is below the mind; Spirituality is beyond the mind
    112. 112. Other Diagnostic Tools -2Radionuclide SPECT Scanning1PET Scanning2Transesophageal Echocardiography3 1. AJNR Am J Neuroradiol. 2001 May;22(5):928-36 2.Neuroimaging Clin N Am. 2003 Nov;13(4):741-58 3. Heart Dis. 2003 Sep-Oct;5(5):320-2 Success is a prize to be won. Action is the road to it. Chance is what may lurk in the shadows at the road side.
    113. 113. THERAPEUTIC MYTHS Evidence based medicine = Randomized Clinical Trials – Best Research Evidence – Clinical Expertise – Patient Values Systematic Escalation of anti thrombotic therapy Brain Hemorrhage Demands Neuro surgical Consultation
    114. 114. Thrombolysis in acute strokeDead/dependent follow-up 62% vs 69% s.Deaths by day 14 22% vs 12% s.Deaths during follow-up 22% vs 19% s.Deaths ordered by antithrombotic 40% 30% 17% 10%Deaths ordered by thrombolytic 3% 20% ns.Deaths ordered by stroke severity 11% 29% ns.Symptomatic ICH by 14 dys 9.3% vs 2.5% s.Fatal ICH by 14 dys 6% vs 1% s.Dead/dependent follow-up < 3 hr. 55% vs 71% s.!Dead follow-up < 3 hr. 20% vs 25% ns. NATURE, TIME AND PATIENCE are the 3 great physicians
    115. 115. NINDS ConsensusDoor to MD evaluation 10 minDoor to CT completion 25 minDoor to CT read 45 minDoor to treatment 60 minAccess to neurological expertise 15 minAccess to neurosurgical expertise 2 hrsAdmit to monitored bed 3 hrs Memory, Pity and Beauty are short lived in life; But tinged with emotion persist in life
    116. 116. CONCLUSION • MYTHS • PITFALLS • PROGNOSTIC PEARLSIt is the disease of not listening, the malady of not marking, that I am troubled withal - Shakespeare
    117. 117. CVD – Prevention or Cure?While number of curative methods are available, preventive therapy is undoubtedly the main strategy in the management of CVD Lijec Vjesn. 2003 Nov-Dec;125(11-12):322-8 The sign wasn’t placed there By the Big Printer in the sky
    118. 118. Where are we ……? Call Stroke onset emergency Secondary prevention services Full recovery U RS Activated (15 minutes) Neuroprotective drug infusedDrugs administered ‘stroke-treatment’ 6-8 O during transport cocktail H ER stroke team Brain scan The art of medicine is caring for the heart of the patient
    119. 119. Dedicated to my family formaking everything worthwhile
    120. 120. READ not to contradict or confute Nor to Believe and Take for Granted but TO WEIGH AND CONSIDER THANK YOUMy sincere thanks to Thudhimugan .K for his meticulous computer work

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