This document discusses pain pathways and the neural circuitry of pain. It notes that pain is a complex response involving both physiological and psychosocial factors. Critically ill patients commonly experience moderate to severe acute pain from their medical conditions and procedures. Inadequately treated acute pain in critical illness can increase the risk of developing chronic pain after discharge and contribute to poorer health outcomes. The document outlines evidence that social support can help reduce both physical and social pain responses in the brain.
This document discusses central sensitization, a condition where the central nervous system amplifies sensory processing, resulting in hypersensitivity and chronic pain. It begins by explaining how acute pain becomes chronic pain due to central sensitization. It then describes the mechanisms of central sensitization, including wind-up in the spinal cord, impaired descending pain inhibition, and changes in the brain. It discusses how central sensitization can be assessed through measures like conditioned pain modulation, exercise-induced analgesia, and hypersensitivity questionnaires. The document provides criteria for identifying central sensitization in musculoskeletal pain patients and signs and symptoms of central sensitization. It concludes by discussing treatment implications when central sensitization is present.
This document discusses central sensitization (CS), including its recognition and implications for physiotherapy. It defines CS and reviews evidence that CS can be assessed using questionnaires, quantitative sensory testing, and factors like temporal summation. Management of CS may include education, cognitive approaches, TENS, exercise and medications targeting central pain processing. The document provides tips for physiotherapists in managing patients with CS, such as using appropriate pressures and treatment windows, addressing pain behaviors and beliefs, and taking a multidisciplinary approach.
Dr. Gavin Pattullo discusses updates in pain management. The opioid crisis highlights the need for non-opioid options to manage pain. The IASP definition of pain distinguishes between nociception and pain. The primary pain management strategy is to stop nociception using neural blockade and NSAIDs/COX-2 inhibitors. Effective pain assessment evaluates dynamic pain relief, analgesia, sensory analgesia, and opioid sparing. A strategic approach to pain addresses both the sensory and affective components, starting with blocking nociception before considering pharmacological or non-pharmacological options to treat the affective aspect.
The document summarizes a seminar presentation on the antinociceptive activity of the ethanolic extract of Pachyptera hymenaea leaves in animal models of neuropathic pain. The presentation introduces neuropathic pain and various animal models used to study it, including sciatic nerve ligation, chronic ethanol consumption, and cisplatin injection. The objectives are to evaluate the extract's antinociceptive effects in these models. Methods describe preparing the extract, inducing neuropathic pain, and evaluating effects using tail flick and hot plate tests. Results found the extract showed significant antinociception in both tests across models at doses of 25 and 50 mg/kg, indicating potential as a treatment for neuropathic pain.
The document discusses neuropathic pain, defining it and differentiating it from other types of pain. It provides statistics on the prevalence of acute and chronic pain. Neuropathic pain is very common, affects 1 in 7 people in the UK, and has both acute and chronic time courses. It has a massive socioeconomic impact. Treatment involves multiple modalities including pharmacological, physical, and psychological approaches.
Neuropathic pain is caused by damage or disease of the somatosensory nervous system. It is estimated to affect around 9% of the general population. Neuropathic pain has a significant burden and can reduce quality of life more than death for some patients. Conditions associated with nerve damage, such as diabetes and HIV, are increasing globally. While first-line treatments for neuropathic pain like antidepressants and anticonvulsants can provide some relief, their effects are limited. More research and access to existing treatments is still needed to help manage this challenging problem.
Neuropathic pain:
- Affects 1-8% of the general population, but is more common in specific groups like those with diabetes, HIV, or spinal cord injuries.
- Has a significant negative impact on quality of life, mobility, employment, and mental health for those affected.
- Places a large burden on healthcare systems and society. The prevalence of neuropathic pain is expected to rise due to increasing rates of conditions like diabetes mellitus.
This document discusses central sensitization, a condition where the central nervous system amplifies sensory processing, resulting in hypersensitivity and chronic pain. It begins by explaining how acute pain becomes chronic pain due to central sensitization. It then describes the mechanisms of central sensitization, including wind-up in the spinal cord, impaired descending pain inhibition, and changes in the brain. It discusses how central sensitization can be assessed through measures like conditioned pain modulation, exercise-induced analgesia, and hypersensitivity questionnaires. The document provides criteria for identifying central sensitization in musculoskeletal pain patients and signs and symptoms of central sensitization. It concludes by discussing treatment implications when central sensitization is present.
This document discusses central sensitization (CS), including its recognition and implications for physiotherapy. It defines CS and reviews evidence that CS can be assessed using questionnaires, quantitative sensory testing, and factors like temporal summation. Management of CS may include education, cognitive approaches, TENS, exercise and medications targeting central pain processing. The document provides tips for physiotherapists in managing patients with CS, such as using appropriate pressures and treatment windows, addressing pain behaviors and beliefs, and taking a multidisciplinary approach.
Dr. Gavin Pattullo discusses updates in pain management. The opioid crisis highlights the need for non-opioid options to manage pain. The IASP definition of pain distinguishes between nociception and pain. The primary pain management strategy is to stop nociception using neural blockade and NSAIDs/COX-2 inhibitors. Effective pain assessment evaluates dynamic pain relief, analgesia, sensory analgesia, and opioid sparing. A strategic approach to pain addresses both the sensory and affective components, starting with blocking nociception before considering pharmacological or non-pharmacological options to treat the affective aspect.
The document summarizes a seminar presentation on the antinociceptive activity of the ethanolic extract of Pachyptera hymenaea leaves in animal models of neuropathic pain. The presentation introduces neuropathic pain and various animal models used to study it, including sciatic nerve ligation, chronic ethanol consumption, and cisplatin injection. The objectives are to evaluate the extract's antinociceptive effects in these models. Methods describe preparing the extract, inducing neuropathic pain, and evaluating effects using tail flick and hot plate tests. Results found the extract showed significant antinociception in both tests across models at doses of 25 and 50 mg/kg, indicating potential as a treatment for neuropathic pain.
The document discusses neuropathic pain, defining it and differentiating it from other types of pain. It provides statistics on the prevalence of acute and chronic pain. Neuropathic pain is very common, affects 1 in 7 people in the UK, and has both acute and chronic time courses. It has a massive socioeconomic impact. Treatment involves multiple modalities including pharmacological, physical, and psychological approaches.
Neuropathic pain is caused by damage or disease of the somatosensory nervous system. It is estimated to affect around 9% of the general population. Neuropathic pain has a significant burden and can reduce quality of life more than death for some patients. Conditions associated with nerve damage, such as diabetes and HIV, are increasing globally. While first-line treatments for neuropathic pain like antidepressants and anticonvulsants can provide some relief, their effects are limited. More research and access to existing treatments is still needed to help manage this challenging problem.
Neuropathic pain:
- Affects 1-8% of the general population, but is more common in specific groups like those with diabetes, HIV, or spinal cord injuries.
- Has a significant negative impact on quality of life, mobility, employment, and mental health for those affected.
- Places a large burden on healthcare systems and society. The prevalence of neuropathic pain is expected to rise due to increasing rates of conditions like diabetes mellitus.
1. The document discusses pain, defining it as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
2. Pain is always subjective and can be somatic, visceral, or neuropathic in nature. It can be acute or chronic, with chronic pain lasting over 3 months and having a large psycho-social component.
3. The gate control theory proposes that psychological factors can affect the experience of pain by opening and closing a "gate" in the spinal cord that modulates pain transmission.
This document provides an overview of pain management. It begins with an introduction defining pain and its prevalence in society. It then covers the pathophysiology and classification of different types of pain such as nociceptive, neuropathic, and chronic pain. The clinical presentation of acute and chronic pain is discussed. Treatment options including pharmacological therapies like opioids and non-opioid drugs as well as non-pharmacological approaches are summarized. Specific drugs like morphine are also described in terms of their use, effects, and side effects.
This document discusses acute pain and chronic pain. It defines acute pain as sudden pain caused by a specific event that usually lasts less than 6 months. Chronic pain lasts longer than 6 months and can continue after the original cause has healed. The document outlines the nociceptive pathway and describes how pain signals are transmitted from nociceptors to the spinal cord and brain. It also discusses mechanisms of pain modulation and factors that can lead acute pain to become chronic, such as inadequate pain management allowing central sensitization.
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented At Primed, QE2 Conference Centre, Westminster, London to National Audience of Primary Care Doctors
5th November 2009
1. The document discusses different types of pain including acute pain, neuropathic pain, and chronic pain.
2. It defines acute pain as a normal physiological response to tissue damage, such as from surgery, trauma, or acute illness. Chronic pain persists beyond normal tissue healing time.
3. Neuropathic pain is initiated or caused by primary lesions or dysfunction in the nervous system and can involve both peripheral and central nervous system pathways.
The document discusses pain and psychological perspectives in terminal Motor Neurone Disease (MND) sufferers. It defines terminal illness and MND, describing the physical and psychological pain associated with MND. Regarding physical pain, it discusses types, measurement using scales like the SF-36, and pharmacological and non-pharmacological management approaches. For psychological pain, it covers measurement using tools like the BDI and management methods. The document also addresses comorbidities like depression, desire for death, and suicidal thoughts in terminal MND patients. It concludes that managing pain in terminal illness requires a multidisciplinary approach including both medical and psychological support.
This document provides information on neuropathic pain diagnosis and management, with a focus on diabetic peripheral neuropathy. It discusses:
- The different types of pain (nociceptive, neuropathic, central sensitization) and characteristics of each. Neuropathic pain is caused by damage to the somatosensory nervous system and is often chronic.
- Neuropathic pain is prevalent in many conditions including diabetes, cancer, HIV, post-surgical, and postherpetic neuralgia. Over 50% of people with diabetes experience painful diabetic peripheral neuropathy.
- The pathophysiology of neuropathic pain involves peripheral and central nervous system changes that lead to hypersensitivity and abnormal pain response. Sleep disruption and anxiety/depression can
Dr. Shekhar Anand presented on methods of chronic pain management to the Department of Anesthesiology. He discussed that chronic pain is defined as pain lasting longer than 3-6 months and can be nociceptive, neuropathic, or mixed in nature. Chronic pain is best managed using a multidisciplinary approach including pharmacological interventions like opioids, antidepressants, anticonvulsants, as well as non-pharmacological therapies like cognitive behavioral therapy, physical therapy, and interventional procedures. The goals of chronic pain management are to improve function and quality of life, rather than to cure the underlying cause of pain.
This document discusses chronic pain management. It defines chronic pain as pain that lasts months or years in any part of the body and can lead to depression, anxiety, and sleep issues. Chronic pain differs from acute pain in that it continues long after an injury heals. The document describes three types of chronic pain - neuropathic, somatic, and visceral - and their characteristics. It discusses evaluating and measuring pain, as well as pharmacological, physical, psychological, and invasive treatment methods for managing chronic pain. The goal of chronic pain treatment is to improve daily functioning and quality of life by decreasing pain and suffering through a multidisciplinary approach.
ISMST - 2014 Presentation Final PresentationKenneth Craig
This document summarizes a case series study on the use of extracorporeal shockwave therapy (ESWT) to treat complex/neuropathic pain syndromes. It describes 12 patients who underwent 4 treatments of ESWT at weekly intervals and experienced significant reductions in pain, physical impairment, and emotional distress that were maintained at 24-week follow up based on standardized questionnaires. The proposed mechanisms of action of ESWT for neuropathic pain and rationale for its application are discussed. The study concludes that ESWT shows promise for treating neuropathic pain and warrants further research.
This document discusses chronic pain management. It defines chronic pain as pain lasting over 3 months. It describes different types of pain such as somatic, visceral and neuropathic pain. It discusses various chronic pain conditions like fibromyalgia, complex regional pain syndrome, postherpetic neuralgia and diabetic neuropathy. It covers evaluation of chronic pain, pathophysiology of chronic pain, brain regions involved, and the multidimensional nature of chronic pain including physical, psychological and social factors. Finally, it discusses various management approaches for chronic pain including pharmacological, physical, psychological and invasive techniques.
The document discusses pain management and defines pain as an unpleasant sensory and emotional experience arising from actual or potential tissue damage. It describes various theories of pain including the gate control theory, specificity theory, and pattern theory. It also outlines the physiology of pain, effects of pain, and assessments and strategies for pain management, including both pharmacologic interventions like medications and non-pharmacologic methods like heat/cold therapy, exercise, acupuncture, acupressure, TENS, and relaxation techniques. The nurse's role in comprehensive pain management is also discussed.
This document discusses pain management in oncology. It begins by outlining the objectives of understanding cancer pain management principles, categorizing pain, optimizing analgesia, using adjuvant analgesics, and recognizing when interventional therapies could help. It then provides background on cancer prevalence in Ghana and the high rates of pain in cancer patients. The rest of the document details approaches to assessing and treating cancer pain, including pharmacological and non-pharmacological options. It emphasizes a stepwise approach using the WHO analgesic ladder and treating the specific cause and type of cancer pain.
Sue Barnes - Pain management and Multiple SclerosisMS Trust
This document provides an overview of pain management for patients with multiple sclerosis (MS). It defines different types of pain commonly experienced by MS patients, such as Lhermitte's sign and central neuropathic dysaesthesia. Neuropathic pain is discussed in more detail, including its pathophysiology and diagnosis. Common neuropathic pain medications for MS are presented, including amitriptyline, gabapentin, pregabalin, and opioids. National guidelines for treating neuropathic pain in MS are summarized. Specialist referral is recommended for complex pain or when first-line treatments are ineffective.
Application of Pstim in Clinical Practice MaxiMedRx
The P-Stim and ANSiStim™ miniaturized device is designed to administer auricular point stimulation treatment over several days. The ear provides numerous points for stimulation within a small area. Stimulation is performed by electrical pulses emitted through strategically positioned needles. The ANSiscope device monitors the pain condition of the patient before, during and after the treatment.
The P-Stim and ANSiStim™ point stimulation therapy is mainly used to treat pain. Use of the device is recommended for pre-operative, intra-operative and post-operative pain therapy as well as for the treatment of chronic pain. DyAnsys is researching the possibilities of using this concept for the treatment of depression, addiction and allergy.
P-Stim and ANSiStim™ therapy allows continuous point stimulation over a period of several days while offering the patient a high degree of comfort and mobility. Use of the P-Stim and ANSiStim™ therapy provides advantages over drug therapy by minimizing possible side-effects caused by pain medications (i.e. opioid). In most cases, the patient continues to lead a normal life without side effects or any loss of quality of life.
CHRONIC PAIN AND DEPRESSION: Cause or Effect or Linked?Sudhir Kumar
Chronic pain and depression are both common conditions, and in many patients, they co-exist. This presentation looks at the link between chronic pain and depression. Various drugs that can be used to treat chronic pain/depression have been discussed, with a special emphasis on tricyclic antidepressants.
Nyeri adalah penggabungan perasaan sensorik dan emosional yang dipengaruhi oleh berbagai faktor.
Nyeri memiliki dua dimensi yg jelas, dimensi inderawi dan emosional
Peran dimensi emosional lebih dominan dibanding inderawi utamanya pada nyeri kronik.
Pain is the production (out put ) of the brain.
Pain is invisible disease, we can’t see it like other disease, such as struma, fracture or blind.
What you have to do is to believe what ever the patient says.
Pain is what ever the patient says it is
Pain is invisible diseases, but is real for patient.
1) Pain management involves using the WHO pain ladder to treat pain with mild, moderate, or strong opioids depending on severity. Common opioids include morphine, codeine, oxycodone, and fentanyl.
2) Opioids can cause side effects like constipation, nausea, sedation, and respiratory depression. Doses are increased gradually until pain is controlled.
3) For breakthrough pain, the as-needed dose is typically 1/6 of the total daily opioid dose. Modified release opioids can replace short-acting opioids at the same total daily dose split into fewer doses.
4) If swallowing is difficult, opioids can be given by other routes like intramuscular or continuous
This document discusses addiction, pseudo-addiction, and an integrated approach to pain management. It defines pseudo-addiction as medication-seeking behavior that occurs when pain relief is inadequate, and distinguishes it from true addiction by noting that pseudo-addicted individuals do not seek euphoria and focus on treatment, while addicted individuals do. The document advocates for a balanced, multidisciplinary approach addressing physical, cognitive, emotional, social, and spiritual factors to maximize function and quality of life.
1. The document discusses pain, defining it as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
2. Pain is always subjective and can be somatic, visceral, or neuropathic in nature. It can be acute or chronic, with chronic pain lasting over 3 months and having a large psycho-social component.
3. The gate control theory proposes that psychological factors can affect the experience of pain by opening and closing a "gate" in the spinal cord that modulates pain transmission.
This document provides an overview of pain management. It begins with an introduction defining pain and its prevalence in society. It then covers the pathophysiology and classification of different types of pain such as nociceptive, neuropathic, and chronic pain. The clinical presentation of acute and chronic pain is discussed. Treatment options including pharmacological therapies like opioids and non-opioid drugs as well as non-pharmacological approaches are summarized. Specific drugs like morphine are also described in terms of their use, effects, and side effects.
This document discusses acute pain and chronic pain. It defines acute pain as sudden pain caused by a specific event that usually lasts less than 6 months. Chronic pain lasts longer than 6 months and can continue after the original cause has healed. The document outlines the nociceptive pathway and describes how pain signals are transmitted from nociceptors to the spinal cord and brain. It also discusses mechanisms of pain modulation and factors that can lead acute pain to become chronic, such as inadequate pain management allowing central sensitization.
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented At Primed, QE2 Conference Centre, Westminster, London to National Audience of Primary Care Doctors
5th November 2009
1. The document discusses different types of pain including acute pain, neuropathic pain, and chronic pain.
2. It defines acute pain as a normal physiological response to tissue damage, such as from surgery, trauma, or acute illness. Chronic pain persists beyond normal tissue healing time.
3. Neuropathic pain is initiated or caused by primary lesions or dysfunction in the nervous system and can involve both peripheral and central nervous system pathways.
The document discusses pain and psychological perspectives in terminal Motor Neurone Disease (MND) sufferers. It defines terminal illness and MND, describing the physical and psychological pain associated with MND. Regarding physical pain, it discusses types, measurement using scales like the SF-36, and pharmacological and non-pharmacological management approaches. For psychological pain, it covers measurement using tools like the BDI and management methods. The document also addresses comorbidities like depression, desire for death, and suicidal thoughts in terminal MND patients. It concludes that managing pain in terminal illness requires a multidisciplinary approach including both medical and psychological support.
This document provides information on neuropathic pain diagnosis and management, with a focus on diabetic peripheral neuropathy. It discusses:
- The different types of pain (nociceptive, neuropathic, central sensitization) and characteristics of each. Neuropathic pain is caused by damage to the somatosensory nervous system and is often chronic.
- Neuropathic pain is prevalent in many conditions including diabetes, cancer, HIV, post-surgical, and postherpetic neuralgia. Over 50% of people with diabetes experience painful diabetic peripheral neuropathy.
- The pathophysiology of neuropathic pain involves peripheral and central nervous system changes that lead to hypersensitivity and abnormal pain response. Sleep disruption and anxiety/depression can
Dr. Shekhar Anand presented on methods of chronic pain management to the Department of Anesthesiology. He discussed that chronic pain is defined as pain lasting longer than 3-6 months and can be nociceptive, neuropathic, or mixed in nature. Chronic pain is best managed using a multidisciplinary approach including pharmacological interventions like opioids, antidepressants, anticonvulsants, as well as non-pharmacological therapies like cognitive behavioral therapy, physical therapy, and interventional procedures. The goals of chronic pain management are to improve function and quality of life, rather than to cure the underlying cause of pain.
This document discusses chronic pain management. It defines chronic pain as pain that lasts months or years in any part of the body and can lead to depression, anxiety, and sleep issues. Chronic pain differs from acute pain in that it continues long after an injury heals. The document describes three types of chronic pain - neuropathic, somatic, and visceral - and their characteristics. It discusses evaluating and measuring pain, as well as pharmacological, physical, psychological, and invasive treatment methods for managing chronic pain. The goal of chronic pain treatment is to improve daily functioning and quality of life by decreasing pain and suffering through a multidisciplinary approach.
ISMST - 2014 Presentation Final PresentationKenneth Craig
This document summarizes a case series study on the use of extracorporeal shockwave therapy (ESWT) to treat complex/neuropathic pain syndromes. It describes 12 patients who underwent 4 treatments of ESWT at weekly intervals and experienced significant reductions in pain, physical impairment, and emotional distress that were maintained at 24-week follow up based on standardized questionnaires. The proposed mechanisms of action of ESWT for neuropathic pain and rationale for its application are discussed. The study concludes that ESWT shows promise for treating neuropathic pain and warrants further research.
This document discusses chronic pain management. It defines chronic pain as pain lasting over 3 months. It describes different types of pain such as somatic, visceral and neuropathic pain. It discusses various chronic pain conditions like fibromyalgia, complex regional pain syndrome, postherpetic neuralgia and diabetic neuropathy. It covers evaluation of chronic pain, pathophysiology of chronic pain, brain regions involved, and the multidimensional nature of chronic pain including physical, psychological and social factors. Finally, it discusses various management approaches for chronic pain including pharmacological, physical, psychological and invasive techniques.
The document discusses pain management and defines pain as an unpleasant sensory and emotional experience arising from actual or potential tissue damage. It describes various theories of pain including the gate control theory, specificity theory, and pattern theory. It also outlines the physiology of pain, effects of pain, and assessments and strategies for pain management, including both pharmacologic interventions like medications and non-pharmacologic methods like heat/cold therapy, exercise, acupuncture, acupressure, TENS, and relaxation techniques. The nurse's role in comprehensive pain management is also discussed.
This document discusses pain management in oncology. It begins by outlining the objectives of understanding cancer pain management principles, categorizing pain, optimizing analgesia, using adjuvant analgesics, and recognizing when interventional therapies could help. It then provides background on cancer prevalence in Ghana and the high rates of pain in cancer patients. The rest of the document details approaches to assessing and treating cancer pain, including pharmacological and non-pharmacological options. It emphasizes a stepwise approach using the WHO analgesic ladder and treating the specific cause and type of cancer pain.
Sue Barnes - Pain management and Multiple SclerosisMS Trust
This document provides an overview of pain management for patients with multiple sclerosis (MS). It defines different types of pain commonly experienced by MS patients, such as Lhermitte's sign and central neuropathic dysaesthesia. Neuropathic pain is discussed in more detail, including its pathophysiology and diagnosis. Common neuropathic pain medications for MS are presented, including amitriptyline, gabapentin, pregabalin, and opioids. National guidelines for treating neuropathic pain in MS are summarized. Specialist referral is recommended for complex pain or when first-line treatments are ineffective.
Application of Pstim in Clinical Practice MaxiMedRx
The P-Stim and ANSiStim™ miniaturized device is designed to administer auricular point stimulation treatment over several days. The ear provides numerous points for stimulation within a small area. Stimulation is performed by electrical pulses emitted through strategically positioned needles. The ANSiscope device monitors the pain condition of the patient before, during and after the treatment.
The P-Stim and ANSiStim™ point stimulation therapy is mainly used to treat pain. Use of the device is recommended for pre-operative, intra-operative and post-operative pain therapy as well as for the treatment of chronic pain. DyAnsys is researching the possibilities of using this concept for the treatment of depression, addiction and allergy.
P-Stim and ANSiStim™ therapy allows continuous point stimulation over a period of several days while offering the patient a high degree of comfort and mobility. Use of the P-Stim and ANSiStim™ therapy provides advantages over drug therapy by minimizing possible side-effects caused by pain medications (i.e. opioid). In most cases, the patient continues to lead a normal life without side effects or any loss of quality of life.
CHRONIC PAIN AND DEPRESSION: Cause or Effect or Linked?Sudhir Kumar
Chronic pain and depression are both common conditions, and in many patients, they co-exist. This presentation looks at the link between chronic pain and depression. Various drugs that can be used to treat chronic pain/depression have been discussed, with a special emphasis on tricyclic antidepressants.
Nyeri adalah penggabungan perasaan sensorik dan emosional yang dipengaruhi oleh berbagai faktor.
Nyeri memiliki dua dimensi yg jelas, dimensi inderawi dan emosional
Peran dimensi emosional lebih dominan dibanding inderawi utamanya pada nyeri kronik.
Pain is the production (out put ) of the brain.
Pain is invisible disease, we can’t see it like other disease, such as struma, fracture or blind.
What you have to do is to believe what ever the patient says.
Pain is what ever the patient says it is
Pain is invisible diseases, but is real for patient.
1) Pain management involves using the WHO pain ladder to treat pain with mild, moderate, or strong opioids depending on severity. Common opioids include morphine, codeine, oxycodone, and fentanyl.
2) Opioids can cause side effects like constipation, nausea, sedation, and respiratory depression. Doses are increased gradually until pain is controlled.
3) For breakthrough pain, the as-needed dose is typically 1/6 of the total daily opioid dose. Modified release opioids can replace short-acting opioids at the same total daily dose split into fewer doses.
4) If swallowing is difficult, opioids can be given by other routes like intramuscular or continuous
This document discusses addiction, pseudo-addiction, and an integrated approach to pain management. It defines pseudo-addiction as medication-seeking behavior that occurs when pain relief is inadequate, and distinguishes it from true addiction by noting that pseudo-addicted individuals do not seek euphoria and focus on treatment, while addicted individuals do. The document advocates for a balanced, multidisciplinary approach addressing physical, cognitive, emotional, social, and spiritual factors to maximize function and quality of life.
This document outlines the history of pain theories from the 19th century. It discusses early theorists like Johannes Muller who proposed specific nerve fibers for pain and Maximillian von Frey who identified points on the skin for different sensations. Alfred Goldscheider postulated a cumulative process for pain in the spinal cord and brain rather than specific fibers. Later, William Livingston considered pain a perception rather than just a sensory event and studied psychological aspects of pain. Charles Sherrington coined the term "synapse" and viewed the nervous system as an integrated whole.
This document provides an overview of neonatal ventilator terminology and lung function. It discusses key topics such as respiration, ventilation, oxygenation, lung anatomy including the conducting and respiratory zones, cell types in the respiratory tract, surfactant, perfusion, ventilation, lung volumes, gas exchange, compliance, resistance, and time constant. The document is intended as an introduction for a neonatal ventilator workshop to establish foundational concepts around ventilator support and lung function in neonates.
This document provides an outline for the care of critically ill patients. It begins with definitions and notes that critically ill patients require intense nursing care and monitoring of medical and surgical treatment. It describes the anatomy, etiologies, signs/symptoms, investigations and management considerations for treating critically ill patients. Specific conditions that may require intensive care such as acute respiratory failure, sepsis, and congestive heart failure are also discussed. The treatment section emphasizes multisystem support and monitoring to stabilize the patient until the underlying condition can be addressed.
This document summarizes the pain pathway in the human body. It begins with an introduction to pain and its characteristics. It then discusses the different types of pain sensations conducted by different nerve fibers. It explains Gate Control Theory and the differences between somatic and visceral sensory function. It provides details on pain receptors, the pathway of sensory impulses from receptors to the brain, and examples of tooth pulp pain and referred pain. It concludes with management strategies for pain.
The document discusses several theories of pain including:
1) Specificity theory which proposed specialized pain receptors
2) Gate control theory which proposes that pain is modulated by a "gate" in the spinal cord that can be opened or closed by non-painful stimuli
3) Neuromatrix theory which suggests that a person's unique matrix of neurons is shaped by their physical, psychological, and cognitive traits and experiences.
It also discusses pain control mechanisms like endogenous opiates and placebos, and provides examples of how integrating pain theories can guide multimodal pain management strategies.
This document provides an overview of pain theories and the Gate Control Theory of pain modulation. It defines pain and classifies types of pain fibers and pain. Several historical theories of pain are outlined. The bulk of the document focuses on explaining the Gate Control Theory proposed by Melzack and Wall in 1965. This theory proposes that a gating mechanism in the dorsal horn of the spinal cord regulates whether painful stimuli are transmitted to the brain based on the interplay between small nerve fibers carrying pain and large fibers carrying other sensations. When the gate is closed, pain is not perceived, and when open, pain signals pass through.
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
The gate control theory of pain proposes that a "gate" in the spinal cord can open and close to modulate pain perception. It suggests that non-painful stimuli can close the gate and inhibit pain transmission, while painful stimuli open the gate and facilitate pain transmission. Psychological factors are also thought to influence the gating mechanism by modulating the balance of activity between small and large diameter nerve fibers.
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
Response To Pain, Carl Graham, Clinical Psychologist, Pain Medicine Unit, Fre...ArthritisNT
This document discusses various concepts related to chronic pain management including stress response, escape behaviors, central sensitization, attention, mood, inflammation, controllability, expectancy, relaxation, and behavioral neuromodulation. The key goals are pacing oneself, managing distress, learning not to avoid activities due to fear of pain, and incorporating rest while gradually increasing engagement in meaningful and pleasurable activities.
Dr. Nilesh Kate gives a lecture on pain physiology covering definitions of pain, types of pain like fast and slow pain transmitted by different nerve fibers, varieties of pain including acute, chronic, cutaneous, deep somatic, and visceral pain. Referred pain and its mechanisms like convergence and dermatomal theories are explained. The pathways of pain from transduction to transmission, perception, and modulation in the central nervous system are outlined.
This document provides an overview of pain and pain pathways. It defines pain, discusses the history of pain theories, and describes the different types of pain receptors and neural pathways involved in pain perception and modulation. Specifically, it outlines fast and slow pain pathways conducted by myelinated and unmyelinated fibers, discusses peripheral and central mechanisms of injury-induced pain, and classification of pain including somatic and visceral pain.
This document discusses pain in several sections:
1. It defines pain and its subjective nature. Pain is the most common reason people seek medical care and acts as a protective mechanism.
2. It describes pain transmission and the gate control theory of pain. Nociceptors transmit pain impulses and can be modulated by other stimuli.
3. It categorizes acute, chronic, and cancer-related pain and discusses factors influencing individual pain responses. Non-pharmacological and pharmacological pain management strategies are also outlined.
1. The document discusses the anatomy and pathways of the pain sensation system. It describes how nociceptors detect painful stimuli and transmit signals to the spinal cord and brain.
2. The spinal cord plays an important role in pain processing. It contains ascending tracts that carry pain signals to the brain and descending tracts that modulate pain. Key nuclei in the spinal cord dorsal horn relay and modulate pain transmission.
3. Pain signals are transmitted from the spinal cord via the spinothalamic tract to the thalamus and then to regions of the cerebral cortex involved in pain perception and modulation like the somatosensory, cingulate, and insular cortices. The periaqueductal
lower, upper and middlepain-management-2010.pptAfframHspt
This document provides an overview of pain management in the geriatric population. It discusses that pain is undertreated in elderly patients due to barriers like comorbidities, polypharmacy, and practitioner bias. The document differentiates between nociceptive, neuropathic, somatic, and visceral pain and how this impacts treatment. Both pharmacological and non-pharmacological approaches to pain management are covered. Common pain conditions in elderly patients and age-related changes that impact pain perception are also reviewed.
This document discusses pain pathophysiology and classifications. It defines pain and describes the pain mechanism, involving etiological factors, pain syndromes, and classifications including acute vs chronic pain. It further describes the three main types of pain - nociceptive, neuropathic, and psychogenic - and provides details on nociceptive and neuropathic pain, their causes, characteristics, and clinical examples.
This document discusses pain management in cardiac surgery. It begins with an overview of pain and its assessment, including different scales used to measure pain intensity. It then discusses factors that can cause pain after cardiac surgery, including sternotomy sites and chest tube insertion. Effective pain management is important for patient outcomes and recovery. The document reviews the pain pathway and different approaches to treating pain, including opioids, regional techniques, and multimodal analgesia. It provides details on specific opioids like morphine, fentanyl, and sufentanil that are commonly used in cardiac surgery.
1. Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is mediated through peripheral sensory nerves and transmitted through the spinal cord and brain.
2. Pain can be classified based on its underlying mechanism as nociceptive, neuropathic, or mixed. Neuropathic pain occurs as a direct result of damage or dysfunction of the nervous system.
3. Pain is also classified based on duration as either acute pain, which resolves with healing, or chronic pain, which persists longer than 3 months and is associated with disability and mood changes. Chronic pain often requires a multidisciplinary treatment approach.
assessment and physiotherapy management of pain in elderly sunil JMI
1. Pain assessment in elderly patients requires a comprehensive evaluation of sensory, emotional, functional, and social impacts of pain. It also requires consideration of age-related changes and beliefs about pain.
2. A thorough history and physical exam are needed to identify potential causes of pain and evaluate for comorbidities. The history should address location, intensity, descriptors, relieving/aggravating factors, and impact on sleep, function, mood and quality of life.
3. Physical exam includes general exam, specific pain evaluation, neurological and musculoskeletal exams to identify potential causes and contributing factors. Assessment of psychological and cognitive factors is also important.
This document discusses assessment and management of pain in the elderly. It defines pain and describes the physiology of pain transmission through nociceptors and nerve fibers. Pain can be acute, chronic, nociceptive, or neuropathic. Chronic pain is common in older adults and has many negative impacts. A comprehensive geriatric pain assessment evaluates multiple factors, including sensory experience, emotional impact, functional status, sleep, attitudes, coping, and goals of treatment. Proper assessment requires a thorough history, physical exam, and diagnostic tests.
Pain Management (General concepts and primary discussions)Saeid Safari
This document provides an overview of pain medicine. It defines pain and discusses its epidemiology, economics, and physiological effects. It describes acute and chronic pain, including their presentations and pathophysiology. Neuropathic and nociceptive pain are major categories discussed. Pain pathways and the gate control theory of pain are also summarized. Psychiatric comorbidities with chronic pain are noted.
Unrelieved pain can have negative physiological effects. It prolongs the stress response and causes harmful changes to the endocrine, cardiovascular, respiratory, immune, and other body systems. Assessing pain in all patients, including those who cannot self-report, is important for effective pain management. A comprehensive pain assessment evaluates location, intensity, quality, onset/duration, relieving/aggravating factors, function, goals, and other details. Non-pharmacological and pharmacological methods are both used to treat pain, and opioids carry side effects like respiratory depression that require monitoring.
This document provides an overview of pain, including its definition, classification, transmission pathways, and management. It begins with defining pain and discussing its incidence and epidemiology. Pain is then classified based on its source, duration, and transmission. The pathways of pain transmission from nociceptors to the central nervous system are explained. Finally, the document discusses pain assessment, management guidelines, and concludes with references.
Chronic pain is common. If we don’t suffer from it ourselves, chances are we know someone who does. Changes in the structure and function of the brain are thought to underlie chronic pain. The good news is that these changes are not hardwired. Many things can be done to influence how the brain processes pain signals including exercise, healthy eating, and better sleep, as well as thinking more adaptive thoughts, positive emotions, and feeling love and connected. This session will highlight the neuroscience related to chronic pain and how engaging in simple self-management strategies can result in less pain and a more rewarding life.
This presentation comes from the Spring Patient Education conference presented by the Scleroderma Patient Education Conference presented by the Scleroderma Foundation of Greater Chicago.
Chronic pain is common. If we don’t suffer from it ourselves, chances are we know someone who does. Changes in the structure and function of the brain are thought to underlie chronic pain. The good news is that these changes are not hardwired. Many things can be done to influence how the brain processes pain signals including exercise, healthy eating, and better sleep, as well as thinking more adaptive thoughts, positive emotions, and feeling love and connected. This session will highlight the neuroscience related to chronic pain and how engaging in simple self-management strategies can result in less pain and a more rewarding life.
This presentation comes from the Spring Patient Education conference presented by the Scleroderma Patient Education Conference presented by the Scleroderma Foundation of Greater Chicago.
Pain is a complex multidimensional experience that is subjective. It involves sensory, cognitive, affective, and behavioral components. Pain is the most common complaint of critically ill patients and is difficult to assess in the ICU due to impaired communication and various barriers. Adequate pain management is important for patient outcomes and involves both pharmacological and non-pharmacological approaches. Sedation is also challenging in the ICU and aims to balance patient comfort and safety while avoiding over sedation.
1. Pain is a complex, subjective experience influenced by physiological, psychological, social, and cultural factors.
2. Accurate pain assessment is crucial for nurses and includes gathering subjective reports from patients, which are the primary source of data.
3. A nurse's key role is as a patient advocate for comprehensive pain management, including both pharmacological and non-pharmacological interventions tailored to each patient's individual experience of pain.
1. Pain is a complex, subjective experience influenced by physiological, psychological, social, and cultural factors.
2. Accurate pain assessment is crucial for nurses and includes gathering subjective data from patients.
3. A nurse's key role is advocating for patients by assisting with pain management through both nonpharmacological and pharmacological interventions.
The document discusses the concept of pain, including its definition, physiology, and theories. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. The physiological processes of pain include transduction, transmission, perception, and modulation. Pain is also categorized by duration (acute or chronic) and pathological condition. The gate control theory proposes that pain impulses can be regulated by a gating mechanism in the central nervous system. Factors like stress and exercise can influence individuals' pain thresholds. A thorough pain assessment considers intensity and other influencing factors.
The document discusses the concept of pain, including its definition, physiology, and theories. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. The physiological processes of pain include transduction, transmission, perception, and modulation. Pain is also categorized by duration (acute or chronic) and pathological condition. The gate control theory proposes that pain impulses can be regulated by a gating mechanism in the central nervous system. Effective pain management requires a thorough assessment of the patient's description of their pain and influencing factors.
This document provides guidelines on chronic pelvic pain. It begins with background on definitions of pain from the World Health Organization, including nociceptive vs. neuropathic pain and acute vs. chronic pain. It describes the innervation of the urogenital system and methods for pain evaluation and measurement. It then covers specific chronic pelvic pain syndromes like chronic prostate pain, bladder pain syndrome, scrotal pain, and urethral pain. It discusses pelvic pain in gynecological practice and neurological aspects. It also covers neurogenic conditions, pelvic floor function and dysfunction, psychological factors, and general treatment approaches.
This document summarizes research on central nervous system (CNS) changes associated with endometriosis. It discusses 1) changes in brain function seen with functional MRI and PET scans, 2) alterations in brain structure with decreases in grey matter volume, 3) decreased activity of the hypothalamic-pituitary-adrenal axis, 4) increased psychological distress, and 5) autonomic nervous system changes. These CNS changes may amplify or generate pain independently and help explain disparities between disease extent and pain levels as well as pain that persists after treatment. Future treatments may need to target both peripheral and central pain mechanisms.
Chronic pains are highly prevalent conditions that are often linked through metaflammation and lifestyle factors. When pain becomes chronic, it undergoes pathological changes including sensitization of the peripheral and central nervous system. Effective management of chronic pains requires a multimodal approach that addresses both the source of pain and pain control through non-invasive and minimally invasive methods before considering more aggressive options.
Similar to Salon 1 14 kasim 09.30 10.30 eli̇zabeth papathanassoglou (20)
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. Aim
• To discuss evidence on:
• a) the neural circuitry of nociception (sensory
and affective pathways),
• b) the diverse mediators elicited in pain, as
well as the downstream intracellular signaling
and pertinent cellular outcomes.
3. Pain/ nociception
• Complex alarm system aiming to promote
survival, healing & adaptation (physical &
psychosocial).
• Can become maladaptive
• Highly integrated neuro-physiological and
psycho-social response
– Not only about injury
– How others react to pain
– Emotional responses
4. Acute Persistent Pain
in critical illness
• #1 stressor recalled by critically ill
patients
• Intricate problem due to limitations
in patient communication
• The majority of critically ill patients
reports pain
• 4 in every 6 critically ill patients
experience moderate to severe
pain
(Puntillo et al., 2014).
• Pain is attributed to
pathophysiological processes and
routine procedures
(Puntillo 1990-2013, Barr 2013)
5. Transition to chronicity:
post-ICU syndrome
• Risk factor for the post-intensive care syndrome:
– “new or worsening impairments in physical, cognitive
or mental health status arising after critical illness and
persisting beyond acute care hospitalization”
(Davidson et al., 2013).
6. Pain Pathways
1ary, 2ary somatosensory
cortexes,
posterior insula
(discriminative aspects of
pain)
dACC
anterior insula
limbic system
7. Sedation suppresses cognition
NOT neural circuitry of pain
1ary, 2ary somatosensory cortexes
anterior insula
dACC posterior insula
limbic system
TMN
9. Inflammation is emotionally
painful too
• Inflammation increases negative affect and
social pain:
– Healthy volunteers exposed to endotoxin showed
an increase in feelings of social disconnection and
neural sensitivity to social pain
Eisenberger et al., 2010
Critically ill patients may
get entrapped in a vicious
circle of heightened
physical and social pain
11. Mitochondrial alarm molecules
(alarmins, DAMPs)
• Upon intense
organismic stress, the
mitochondrion releases
primitive peptides
(DAMPs, alarmins)
• They convey alarm
signals within the cell
(nucleus) and inter-cellularly
promoting
inflammation
12. HMGB-1 (high-mobility group Box-1)
• Alarm nuclear molecule
• Released from distressed and damaged cells
• Secreted by ΜΦ, NK, endothelial, neuron &
glial cells
• Mediator of innate and specific immunity
• It binds to DNA and commences the
inflammatory cascade
• Involved in hypersensitivity and pain
responses
– Agalave & Svensson, 2014
13. HMGB-1
Involved in every aspect
of sepsis and MODS
pathophysiology
– Inflammation
– Cell death
– Organ PMN infiltration
– Oxidative stress
Elicits secretion of TNF
& Cytokines
-feeds back to exaggerated
inflammation state
Wang et al., 1999, Science; 285.
17. Pain affects immunity
• Acute pain in experimental
models causes suppression of
splenic NK activity
(Sakaue, et al., 2011)
• Adequate pain control: inhibits
the expected supression of
lymphoproliferation and of
reduction of NK activity
(Sacerdote et al, 2000; Pollock et al 1991; Page
et al, 2001)
• Chronic pain: ↓cytotoxic CD8+
lymphocytes ↓T-helper type 1
response. ↓NK activity
(Kaufmann, Eisner, et al, 2007; Brennan 1994)
18. Pain promotes cell death
• Persistent pain activates the
JNK pathway
• JNK is a stress-activated
pathway implicated in
inflammation and apoptosis
Gao & Gi, 2008
19. Pain ratings in critically ill patients associate
with death molecules on T and B cells
Papathanassoglou et al (in press)
20. Pain intensity associates with
circulating cell death markers
• Pain intensity correlates with sFas
(r=0.385, p=0.001) and sFasL
(r=0.268, p=0.011) (controlled for
disease severity) in critically ill
patients with and without apparent
tissue injury.
• Significant increases in sFas 30
min after sedation break (p=0.013),
• Significant differences between the
two groups (p=0.031).
WFCCN Congress, 2013
Kletsiou & Papathanassoglou (in press)
21.
22. Pain: it’s no metaphor
• “Pain” of loss and isolation
activates the 2ary
somatosensory cortex
similarly to physical pain
(Kross et al., 2011).
• Analgesic agents
(acetaminophen) also
reduce social pain
(Dewall et al., 2010).
(Kross et al., 2011).
23. Social Isolation is Painful!
• The affective pathway of
nociception gets activated even
by simple social exclusion
conditions, such as being
ignored or excluded from a
game.
• Patients that feel isolated,
lonely or ignored may be at risk
for higher pain intensity, as well
as lower pain threshold.
Eisenberger et al., 2003
24. Social support:
a universal painkiller
• Individuals with more social support show attenuated
neural responses to social exclusion
Masten et al., 2012
• Presence of a significant other lowers pain intensity and
sensitivity and decreases pain-related neural activation
–Montoya et al., 2004
25. Family pictures!
• Viewing pictures of one’s partner
appears to lower the intensity of pain
Eisenberger et al., 2011
26. Pain & Agression
• inadequate analgesia is linked to the
onset of delirium
Robinson & Volmer, 2010
• Interconnection between pain,
agitation and delirium
Barr et al., 2013
• Interpretable in evolutionary terms:
when harmed one may need to
defend oneself and attack.
• Social exclusion, by activating overlapping neural
pathways may also trigger defensive/ aggressive behavior
Warburton et al., 2006
27. Chronic pain post-ICU
• ICU pain commonly persists after
discharge
[Kyranou & Puntillo, 2012]
• Pain frequency, intensity higher in
survivors of ARDS and severe sepsis
[Dowdy et al., 2006; Zimmer at al 2006]
• Surgical ICU patients: At 8 years, pain
and discomfort in 57%
[Timmers et al., 2011]
• General ICU patients: 6 -12 months
post-ICU, chronic pain was reported
by 44% of respondents. shoulder was
the most commonly reported joint
affected (22%).
[Battle et al., 2013]
28. Transition to chronicity:
neurophysiological evidence
• Fear of pain, may be important for the
transition to chronicity.
• The amygdala integrate negative
emotion, anxiety and nociceptive
information
• Amygdalic hyperactivity during early
stages of pain contributes to pain
persistence and chronicity
(Li et al., 2013).
29. Prevention of pain persistence &
chronicity
• Early detection and management
• Early psychological and social support
30. Conclusion
• Cellular responses to persistent
pain may put critically ill
patients at risk for sepsis and
multiple organ dysfunction.
• Social support and emotion are
important in modulating both
acute and persistent pain in
critically ill patients, as well as
the transition to chronic pain
therefore they need to be
targeted specifically in order to
improve patient outcomes.
To discuss evidence on…. From the viewpoint of critically ill patients’ outcomes
The perception of pain is a complex alarm system aiming to promote survival, healing & adaptation, both physical as well as psychosocial.
I want to highlight how highly integrated a phenomenon pain is, which is at the same time a neuro-physiological and psycho-social response, and what are the implications of this for critically ill patients
Pain is not only about tissue injury, it is about emotions, but also about how others react to it. It is actually a complex psychosocial phenomenon.
For the sake of this presentation I would like us to bracket for a little bit everything we know about pain, either being professional knowledge and/ or personal experience, and just follow the line of evidence, in order to realize how highly integrated a phenomenon pain is, which is at the same time a neuro-physiological and psycho-social response.
Recently, pain has been recognized as a risk factor for the post-intensive care syndrome which encompasses “new or worsening impairments in physical, cognitive or mental health status arising after critical illness and persisting beyond acute care hospitalization” (Davidson et al., 2013).
It has long been recognized that pain has both sensory and affective components, Early clinical observations alluded to the existence of separate neural circuitries, since thalamic lesions that inhibit nociception may still leave one’s emotional and autonomic response to pain intact, despite inability to “sense” pain (Jaillard and Ropper, 2013). Further, lesions at the insula or cingulate cortex that inhibit emotional responses to pain render individuals indifferent to the experience of pain despite their ability to sense and localize pain (Foltz and White, 1968; Berthier et al., 1988).
More recently functional magnetic resonance imaging (fMRI) studies showed two components of the neural pathway for physical pain: a sensory component in the primary and secondary somatosensory cortexes and posterior insula coding for discriminative aspects of pain, and an affective component involving the dorsal anterior cingulate cortex (dACC), anterior insula and the limbic system (Eisenberger, 2012).
What is important to note is that these two systems feed back to each other. Even more remarkably, the sensory and affective pathways are activated not only by physical noxious stimuli (eg burn or injury), but also by psychosocial noxious stimuli (eg rejection).
It is important to note here, that By virtue of where these brain structures are localized it is evident that although sedation can suppress cognitive recollection of pain, it cannot effect the neural circuitry of pain which gets triggered either in sleep or wakefulness alike.
For example, sedatives produce their sedative effect by locking on to a specific type of neurotransmitter receptor in the tuberomammillary nucleus TMN called GABA-A, which really does not affect at all the pain pathway
That means that critically ill patients may be in pain and their stress systems activated as a result of pain, although we are unable to observe any signs of pain, and even they will not be able to remember being in pain later.
So the experience of pain is mediated by two distinct, yet highly interactive pathways which constantly feed back to each other and produce more of the conditions that enhance pain perception.
For example, activation of the sensory pathway results in specific intracellular signaling which promotes inflammation and cellular stress which produce even more noxious stimuli
At the same time activation of the affective pathway, produces a stress response which feeds back to intracellular signaling and with the ensuing release of cytokines and neuropeptides augments the perception of pain.
Moreover, the inflammatory response appears to feed back to the affective pathway and to increase negative affect and social pain as well
Healthy volunteers that were exposed to endotoxin vs., placebo showed an increase in feelings of social disconnection and neural sensitivity to social pain (Eisenberger et al., 2010).
Based on such observations, critically ill patients may get entrapped in a vicious circle of heightened physical and social pain that they mutually feed-back to each other.
Lets have a look at the cellular events downstream the sensory pathway. Here is the picture of a neuron and of synaptic signaling.
Activation starts with increased presynaptic release of nociceptive transmitter-mediators from presynaptic neuron
terminals or glia such as neuropeptides: SP (substance P) or CGRP (calcitonin gene related product); amino acids: Glu (glutamate); neurotrophins: NGF (nerve growth factor)
or BDNF (brain-derived neurotrophic factor); chemokines: fractalkine; or cytokines: TNF (tumor necrosis factor), as examples.
The activation process continues with the postsynaptic stimulation of nociceptors located on neurons or glia that include: GPCRs (G-protein coupled receptors) that bind neuropeptides (e.g. SP and CGRP) and
chemokines (e.g. fractalkine); LGICs (ligand-gated ion channels) that bind amino acids (e.g. Glu); NTR (neurotrophin receptor) tyrosine kinases that bind the neurotrophins (e.g. NGF and BDNF) and cytokine receptors that bind TNF.
Nociceptor stimulation leads to the activation of various second-messenger signal transduction that converge to ‘‘turn-on’’ MAPKs via phosphorylation, regarded as a key component in nociceptive sensitization. Activation (phosphorylation) of MAPKs, that include ERK, p38 and JNK, leads to transcriptional regulation, such as activation of TREs (transcription factor response elements) on DNA producing gene products, as well as non-transcriptional regulation that together enhances the excitatory properties of nociceptive activation and sensitization
Activation of transcription factors results in the production of cytokines and neuropeptides, that activate more transcription factors, enhance inflammation and feed back to nociceptive signaling. At the same time, cells may undergo oxidative stress and release alarm molecules which also account for transcriptional activation and feeding back to the vicious circle of pain signaling.
MAPK (mitogen-activated protein kinases, originally called ERK, extracellular signal-regulated kinases),
Biochemical and pharmacological assessment of MAP-kinase signaling along pain pathways in experimental rodent models: a potential tool for the discovery of novel antinociceptive therapeutics
Rebecca M. Edelmayer, Jill-Desiree Brederson, Michael F. Jarvis, Robert S. Bitner *
Biochemical Pharmacology 87 (2014) 390–398
PAMPs include things that are unique to bacteria or viruses — cell wall components that are present in bacteria, but not in vertebrate cells, for example; or double-stranded RNA, which is found in lots of viruses but would be unusual in our own cells. “Danger” signals, on the other hand, are indications of cell death — internal components of a cell, for example, that have leaked out as the cell dies. 1 For a while, it looked as if PAMPs were the major signal leading to innate and then adaptive immunity, but more recently it’s become clear that DAMPs are also very important.
The Third International DAMPs and Alarmins Symposium was recently held in Pittsburgh, USA.The aim of this meeting was to introduce the emergent understanding of the danger signals also called alarmins or damage associated molecular patterns (DAMPs) by analogy to the pathogen associated molecular patterns (PAMPs). What brought our attention to this meeting is the recent discovery that TLRs play an important role in the immune response initiated by the DAMPs. The major DAMPs are HMGB1 (high mobility group box protein-1), S100A8/S100A9, heat-shock proteins, uric acid and DNA.
Among these DAMPs, HMGB1 is the most studied as it has been associated with several diseases, including cancer, sepsis, rheumatoid arthritis, stroke and atherosclerosis. HMGB1 is a very abundant nuclear protein expressed in nearly all cell types. In normal conditions, HMGB1 binds to DNA and bends it to facilitate gene transcription. Under stress conditions, such as injury or infection, HMGB1 is released and promotes inflammation. HMGB1 is passively released by necrotic but not apoptotic death of normal cells and actively secreted by a variety of activated immune and non-immune cells.Contrary to many reports, HMGB1 is not a pro-inflammatory cytokine per se. HMGB1 by itself has little or no proinflammatory activity but it binds to mediators of inflammation such as LPS, DNA or IL-1β and induces signaling pathways leading to NF-κB activation thereby potentiating inflammatory responses. Although the signaling pathways elicited by HMGB1 are not fully defined, there is evidence that the triggering occurs via several receptors including RAGE (receptor for advanced glycation end-products), TLR2, TLR4 and TLR9[1]. HMGB1 binds RAGE to regulate migratory responses, but the use of ultrapure recombinant HMGB1 has demonstrated that it does not bind TLR4 (M. Bianchi, oral communication). However, HMGB1 which is released upon LPS-induced TLR4 activation, binds LPS even if present in very small amounts and carries it to TLR4 therefore perpetuating NF-κB activation and inflammation. A similar mechanism was reported for DNA, which is released into the systemic circulation after traumatic shock or injury, and presented to TLR9 by HMGB1[2]. Thus, HMGB1 is not an endogenous ligand for TLRs but an amplifier of TLR-mediated inflammatory responses.
S100A8 (also known as Myeloid-related protein-8, MRP-8) and S100A9 (MRP14) are highly up-regulated in various diseases, such as sepsis, rheumatoid arthritis, inflammatory bowel disease and cancer. These calcium-binding proteins are the most abundant cytoplasmic proteins of neutrophils and monocytes. They are specifically released at sites of inflammation during the activation of phagocytes. S100A8 and S100A9 form complexes in which S100A8 appears to be the active component, while S100A9 modulates the activity of its binding partner. Although the biological functions of these proteins are not completely understood, they seem to depend on interactions with RAGE and TLR4. Similarly to HMGB1, S100A8-S100A9 complexes amplify the LPS-triggered inflammatory responses of phagocytes. But unlike HMGB1 and according to current knowledge, they can bind to both RAGE and TLR4[3].
The list of DAMPs is rapidly increasing with new additions such as granulysin, eosinophil-derived neurotoxin and serum amyloid A (SAA). A recent report suggests that SAA induces inflammation in a TLR2-dependent manner while another report claims that SAA is an endogenous agonist for TLR4[4, 5].
It is clear that DAMPs interact with TLRs, however it is less clear whether they bind to them. Recombinant DAMP proteins may contain traces of lipoproteins or endotoxins that may be sufficent to skew the results.Before this meeting on DAMPs and Alarmins,HMGB1 was thought to be a TLR4 ligand. This highlights how crucial it is to work with DAMP preparations that are totally free of microbial contaminants in order to understand the role of DAMPs in the numerous cellular processes in which they are involved.
Lets have a look at one of these alarm molecules, HMGB1, which has also been studied in relation to sepsis in critical illness.
High-mobility group box 1 (HMGB1), a highly conserved protein previously known as a DNA-binding protein involved in maintenance of nucleosome structure and regulation of gene transcription, was recently found to act as a potent proinflammatory cytokine during infection responses.
So what happens is that pain and inflammation feed back to each other, thus creating the conditions for the onset of multiple organ dysfunction, which is a devastating outcome for critically ill patients.
At the same time, the soup of cytokines, neuropeptides, alarm molecules and oxygen free radicals signal the central nervous system and they elicit central neurotransmitters that augment pain perception and the characteristic sickness behaviour and negative affect. Then the brain signals back to the periphery through production of even more neuropeptides and cytokines. So a new vicious circle is established.
In a model of endotoxemia, passive immunization with anti-HMG-1 antibodies attenuated the development of hypophagia, indicating that HMG-1 is a mediator of sickness behaviour associated with endotoxemia.
Agnello et al 2002
More importantly these events account for both central as well as peripheral sensitization to pain, which is a dual process consisting of activation and sensitization that is ultimately bidirectional and self-perpetuating.
Persistent nociceptive signaling after tissue damage results in activity-dependent plasticity or a progressive increase in the response of the system to subsequent stimulation, such that mildly noxious (painful) stimuli are perceived as more painful and non-painful, and innocuous stimuli may now elicit pain
Lets have a look at pain’s effect on immunity
Although these results are novel they make sense when previous evidence is taken into account.
In this study, in a sample of critically ill patients we observed for the first time associations between the intensity of pain, as measured by 4 different scales, including two behavioral scales- and expression of the death receptor Fas on B cells and cytotoxic T cells.
This is the first time anybody reports associations between pain and apoptotic markers. What can we conclude of that? Simplistically or not, when critically ill patients are in pain, their immune cells die, so off goes immunity and welcome infections.
In another repeated-measures correlational study we observed weaker, but still very significant associations between Pain intensity and soluble apoptotic markers, both sfas and sfasL.
Also…
Which really links these markers to pain and stress
So pain not only precipitates inflammation but also cell death and immunosuppression, which really set the stage for the development of sepsis as well.
Pain is never a metaphor!
Remarkably, even what we consider metaphorical pain with no apparent sensory component, such as social pain of loss and isolation, activates somatosensory neural circuitry similar to physical pain, to the degree that analgesic agents, such as acetaminophen, along with physical pain also reduce social pain (Dewall et al., 2010). Indeed, intense social pain, such as recalling rejection by a romantic partner activates the secondary somatosensory cortex (Kross et al., 2011).
The affective pathway of nociception appears to be activated even by simple social exclusion conditions, such as being ignored or excluded from a game (Eisenberger et al., 2003).
Patients that feel isolated, lonely or ignored may be at risk for higher pain intensity, as well as lower pain threshold.
Remarkably, even viewing pictures of one’s partner appears to lower the intensity of pain (Eisenberger et al., 2011), which provides empirical support for the practice of displaying pictures of family and friends close to the bed of critically ill patients (Macnab et al., 1997).
inadequate analgesia has been linked to the onset of delirium (Robinson & Volmer, 2010)
practice guidelines acknowledge the interconnection between pain, agitation and delirium (Barr et al., 2013)
Pain’s effect on triggering aggression may be interpretable in evolutionary terms, since when harmed one may need to defend oneself and attack.
Similarly, social exclusion, by virtue of activating overlapping neural pathways may also trigger defensive/ aggressive behavior (Warburton et al., 2006).
Therefore, both physical pain control and social support are essential in preventing critically ill patients’ irritability, aggression and delirium.
Lately awareness on chronic pain after discharge from ICU has increased.