Trigger points are hyperirritable spots in taut bands of skeletal muscle that cause local and referred pain. There is debate around whether trigger points are a peripheral or central nervous system phenomenon. The document discusses that referred pain from trigger points is a central phenomenon initiated by peripheral sensitization from the trigger point. Trigger points act as an ongoing source of nociception that can induce central sensitization. However, central sensitization may also promote trigger point activity. Proper treatment of trigger points can reduce central sensitization by decreasing nociceptive input.
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
This document discusses the physiology of pain. It covers topics such as the definition of pain, the dual nature of fast and slow pain, pain stimuli and the nerve pathways that carry pain signals to the brain. It also discusses the brain areas involved in pain perception, pain modulatory pathways, and the neurochemicals involved in pain pathways. The gate control theory of pain and theories on referred pain are also summarized.
The document discusses definitions of pain, pain pathways in the body, and methods of pain control. It defines pain and discusses how our understanding has evolved from focusing on three components of pain pathways to recognizing additional areas involved like the brainstem, thalamus, and cortex. It also outlines acute versus chronic pain, nociceptors, neural inflammation, pain perception thresholds, spinal cord and ascending/descending pain pathways in the body. Finally, it provides an overview of various primary, secondary, interventional and psychological methods for controlling pain.
This document discusses pain pathophysiology and management. It describes how the pain sensory system detects and responds to tissue damage to protect the body. Pain signals are transmitted via nociceptors in the peripheral nervous system and ascend through the spinal cord and brainstem to the thalamus and cortex. Central pathways can modulate pain transmission both inhibitively and facilitatively. Neuropathic pain can occur when the peripheral or central nervous system is damaged and causes abnormal pain signaling and hypersensitivity. Effective pain management requires understanding these complex physiological mechanisms.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Pain and its treatment in psychiatric practice (2) (1)Adonis Sfera, MD
This document discusses chronic pain from both a historical and medical perspective. It defines acute versus chronic pain and nociceptive versus neuropathic pain. It describes how chronic pain involves central sensitization and can become a way of life. The relationship between pain and conditions like depression is complex. The medicalization of chronic pain through drugs like aspirin changed views of chronic pain. Currently, there are controversies around balancing treating pain while reducing risks of prescription drug abuse and addiction. Serotonin-norepinephrine reuptake inhibitors have been approved to treat some chronic pain disorders.
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.
Central sensitization refers to increased responsiveness of the central nervous system to sensory input. It involves plastic changes in the brain and spinal cord due to peripheral input and neuronal remodeling. This includes long term potentiation and long term depression at synapses, neuroanatomic spreading, and changes in neurochemistry, immunology, and sensory processing in the brain and spinal cord. Central sensitization can amplify pain signals and lead to chronic pain conditions.
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
This document discusses the physiology of pain. It covers topics such as the definition of pain, the dual nature of fast and slow pain, pain stimuli and the nerve pathways that carry pain signals to the brain. It also discusses the brain areas involved in pain perception, pain modulatory pathways, and the neurochemicals involved in pain pathways. The gate control theory of pain and theories on referred pain are also summarized.
The document discusses definitions of pain, pain pathways in the body, and methods of pain control. It defines pain and discusses how our understanding has evolved from focusing on three components of pain pathways to recognizing additional areas involved like the brainstem, thalamus, and cortex. It also outlines acute versus chronic pain, nociceptors, neural inflammation, pain perception thresholds, spinal cord and ascending/descending pain pathways in the body. Finally, it provides an overview of various primary, secondary, interventional and psychological methods for controlling pain.
This document discusses pain pathophysiology and management. It describes how the pain sensory system detects and responds to tissue damage to protect the body. Pain signals are transmitted via nociceptors in the peripheral nervous system and ascend through the spinal cord and brainstem to the thalamus and cortex. Central pathways can modulate pain transmission both inhibitively and facilitatively. Neuropathic pain can occur when the peripheral or central nervous system is damaged and causes abnormal pain signaling and hypersensitivity. Effective pain management requires understanding these complex physiological mechanisms.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Pain and its treatment in psychiatric practice (2) (1)Adonis Sfera, MD
This document discusses chronic pain from both a historical and medical perspective. It defines acute versus chronic pain and nociceptive versus neuropathic pain. It describes how chronic pain involves central sensitization and can become a way of life. The relationship between pain and conditions like depression is complex. The medicalization of chronic pain through drugs like aspirin changed views of chronic pain. Currently, there are controversies around balancing treating pain while reducing risks of prescription drug abuse and addiction. Serotonin-norepinephrine reuptake inhibitors have been approved to treat some chronic pain disorders.
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.
Central sensitization refers to increased responsiveness of the central nervous system to sensory input. It involves plastic changes in the brain and spinal cord due to peripheral input and neuronal remodeling. This includes long term potentiation and long term depression at synapses, neuroanatomic spreading, and changes in neurochemistry, immunology, and sensory processing in the brain and spinal cord. Central sensitization can amplify pain signals and lead to chronic pain conditions.
This document provides an overview of pain pathophysiology and management. It begins with objectives and introduces topics like neuroanatomy, pathophysiology, types of pain, assessment, and management. It describes how pain is a subjective experience transmitted by nociceptors and modulated by various factors. The neuroanatomy of pain transmission from the periphery to the CNS is outlined. Different types of pain like nociceptive, neuropathic, referred, acute, and chronic are defined. Common pain syndromes and their characteristics are mentioned. Non-opioid and opioid medications as well as non-pharmacological approaches for pain management are summarized.
This document provides information on the nervous system and pain pathways. It discusses how pain signals travel through the nervous system, from nociceptors through the spinal cord and brain. It outlines the roles of different nerve fibers and neurotransmitters in pain signaling and modulation. The document also differentiates between acute and chronic pain, covering signs, symptoms, classifications, and treatment approaches including medications and physical therapies.
The document provides an overview of pain, including its definition, classification, theories, pathways, and assessment tools. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is classified based on duration (acute, chronic), pathophysiological mechanisms (nociceptive, neuropathic), and clinical context. Theories of pain discussed include specificity theory, intensity theory, pattern theory, and gate control theory. Pain pathways involve nociception in the peripheral nervous system and transmission/perception in the central nervous system. Common pain assessment tools are also mentioned.
1. Pain was once thought to be a simple, direct transmission from the periphery to the brain, but it is now understood as a complex, multidimensional experience involving both sensory and emotional components.
2. Key developments included Melzack and Wall's gate control theory introducing central modulation, and the recognition of the placebo effect, showing pain is subject to top-down influences.
3. The neuromatrix theory proposes pain arises from patterns of nerve impulses generated in widely distributed brain regions rather than a single pain center.
Acute pain management & preemptive analgesia (3)DR SHADAB KAMAL
This document discusses acute pain management and pre-emptive analgesia. It defines acute pain as pain caused by actual or potential tissue damage that is usually nociceptive in nature. Acute pain management primarily deals with patients recovering from surgery or acute medical conditions. Pre-emptive analgesia aims to prevent central neural sensitization by administering analgesics before a painful stimulus occurs, which can reduce both acute postoperative pain and the risk of chronic postsurgical pain. The document outlines various treatment approaches for acute pain management, including opioids, non-opioid analgesics, regional anesthetic techniques, and multimodal analgesia.
The document discusses the pathophysiology of pain. It defines pain and describes the three systems - sensory, motivational, and cognitive - that interact to produce the experience of pain. It categorizes pain into somatogenic, psychogenic, acute, and chronic types and discusses their characteristics. It also describes age-related differences in pain perception and the neuroanatomy of pain processing, including the roles of the afferent and efferent pathways and different areas of the central nervous system.
The document discusses various topics related to pain, including definitions, types, causes, symptoms, investigations, and treatments. It defines pain and differentiates it from nociception. It describes acute and chronic pain, as well as types including malignant and non-malignant pain. Physiological pain origins like cutaneous, somatic, and visceral pain are explained. Common and serious causes of pain in different body regions are listed. Investigations and various allopathic and alternative pain treatment methods are also outlined.
The document discusses pain management and analgesia. It outlines the consequences of untreated pain such as wasting, immune suppression, and increased risk of complications. It then covers the physiology of pain, types of pain responses, signs of pain, behavioral responses, and methods of pain assessment. Finally, it discusses various pharmacological agents for perioperative pain management including opioids, NSAIDs, local anesthetics, and other drugs, outlining their mechanisms of action, uses, and potential adverse effects.
Here are some key resources on pain and anxiety control in dentistry:
- Sturdvent - A leading manufacturer of dental equipment for pain and anxiety control.
- Ada's journal on anxiety and pain control - The American Dental Association's journal focused on non-pharmacological approaches.
- Journal on pain management by the American Society of Endodontists - Focuses on managing endodontic pain.
- Journal on pain control in dentistry - Focused specifically on controlling pain during various dental procedures.
- Pickard's manual of operative dentistry - A comprehensive textbook covering techniques for operative dentistry including pain control.
- Pain control in operative dentistry by Dr Ann Elrich - A
This chapter describes the neurological and neurosynaptic pathways for both acute and chronic pain. It also delineates the psychological differences between acute and chronic pain. Finally, it introduces the concept of the specific type of pain associated with a specific tissue type, which is useful in the diagnosis of pain problems. This chapter is the foundation for understanding all subsequent chapters on pain.
- Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It can be acute or chronic.
- Acute pain is sharp and short-lived, while chronic pain is intermittent or constant and lasts longer. Chronic pain is more difficult to treat.
- Pain has protective benefits like warning of injury and preventing further damage, but also has negative impacts. The physiology of pain involves receptors, pathways in the peripheral and central nervous systems, and neurotransmitters like glutamate and substance P. The gate control theory proposes mechanisms of pain modulation in the spinal cord and brain.
Current Update in the Management of Post-operative Neuraxial Opioid-induced P...asclepiuspdfs
This document summarizes the current pharmacological treatments available for managing opioid-induced pruritus caused by spinal opioids in postoperative patients. It discusses the mechanisms by which opioids induce pruritus, including activation of the itch center in the central nervous system and sensitization of peripheral nociceptors. The most useful drugs for treating or preventing pruritus are mu opioid receptor antagonists like naloxone, and mixed kappa opioid agonists/mu antagonists like nalbuphine and butorphanol. Other treatments with some efficacy include 5-HT3 serotonin receptor antagonists, D2 dopamine receptor antagonists, sub-anesthetic doses of propofol, and prophylaxis with mirtazapine
This document discusses pain pathways and treatments for pain. It begins by defining pain according to the IASP and describing the sensory and affective dimensions of pain. It then outlines the ascending pain pathway from peripheral receptors to the cortex. Several descending pain pathways are also described originating from the cortex, thalamus, and brainstem. Common craniofacial pain syndromes and their possible pathways are listed. Surgical and non-surgical treatment options for intractable pain are summarized, including neurostimulation, ablative procedures, and neuromodulation therapies.
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.
This document provides an overview of the physiology of pain. It discusses the definition of pain, the dual nature of fast and slow pain, pain stimuli and receptors, nerve pathways carrying pain signals to the brain, brain areas involved in pain perception, descending pain modulatory pathways, and neurochemicals involved in pain pathways. It summarizes different types of pain such as neuropathic pain and nociceptive pain. The gate control theory of pain and modifications to this theory are also briefly described.
The document discusses pain perception and transmission in the human body. It begins by defining pain and outlining the dual sensory and emotional nature of pain. It then describes how pain signals are transmitted from nociceptors to the spinal cord and brain through A and C nerve fibers. The signals travel through the spinothalamic tract to the thalamus and somatosensory cortex. Descending pathways from the brain can modulate pain perception. The gate control theory of pain is also explained. The document further discusses different types of pain and factors that influence pain experience.
This document discusses pain physiology, treatment options for pain, and common questions about pain. It explains that pain receptors detect potentially harmful stimuli and transmit pain messages to the spinal cord and brain. The brain then processes the pain and can send signals to reduce pain perception. Treatment options discussed include medications, mind-body practices, and self-care activities. Common questions addressed relate to aging and pain, assessing pain levels, medication risks and benefits, and the role of psychological factors in chronic pain.
Pain definition, pathway,analgesic pathway, types of painekta dwivedi
This document provides an overview of pain physiology, including definitions of pain, pain receptors and pathways, and theories of pain modulation. It discusses fast and slow pain fibers, pain transmission through the spinal cord and brain, and endogenous analgesic pathways. The gate control theory of pain is explained in detail. Different types of pain and assessment methods are outlined. Both pharmacological and non-pharmacological pain management approaches are summarized.
This study examined the relationship between falls and muscle strength, flexibility, and balance in 133 postmenopausal women with osteoporosis and 133 without osteoporosis. The researchers found that a significantly higher percentage of women with osteoporosis (51%) reported at least one fall in the previous year compared to women without osteoporosis (29%). Logistic regression analysis showed that lower trunk extension strength and the presence of osteoporosis were associated with an increased risk of falls. Specifically, greater trunk extension strength was associated with a lower risk of falls, while the presence of osteoporosis increased the risk of falls.
This document discusses trigeminal neuralgia (TN), a painful neurological condition that causes severe, sporadic facial pain. It begins with background on TN, describing its distinctive clinical history and pain patterns. The document then covers TN's anatomy and potential pathophysiologies, risk factors, characteristics, treatment options, complications, and prognosis over time. TN is caused by compression or irritation of the trigeminal nerve and presents as sudden, severe facial pain that may be triggered by everyday activities like chewing. While medication can provide initial relief, over time additional treatments like surgery may be needed to control breakthrough pain from this disabling condition.
This document provides an overview of pain pathophysiology and management. It begins with objectives and introduces topics like neuroanatomy, pathophysiology, types of pain, assessment, and management. It describes how pain is a subjective experience transmitted by nociceptors and modulated by various factors. The neuroanatomy of pain transmission from the periphery to the CNS is outlined. Different types of pain like nociceptive, neuropathic, referred, acute, and chronic are defined. Common pain syndromes and their characteristics are mentioned. Non-opioid and opioid medications as well as non-pharmacological approaches for pain management are summarized.
This document provides information on the nervous system and pain pathways. It discusses how pain signals travel through the nervous system, from nociceptors through the spinal cord and brain. It outlines the roles of different nerve fibers and neurotransmitters in pain signaling and modulation. The document also differentiates between acute and chronic pain, covering signs, symptoms, classifications, and treatment approaches including medications and physical therapies.
The document provides an overview of pain, including its definition, classification, theories, pathways, and assessment tools. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is classified based on duration (acute, chronic), pathophysiological mechanisms (nociceptive, neuropathic), and clinical context. Theories of pain discussed include specificity theory, intensity theory, pattern theory, and gate control theory. Pain pathways involve nociception in the peripheral nervous system and transmission/perception in the central nervous system. Common pain assessment tools are also mentioned.
1. Pain was once thought to be a simple, direct transmission from the periphery to the brain, but it is now understood as a complex, multidimensional experience involving both sensory and emotional components.
2. Key developments included Melzack and Wall's gate control theory introducing central modulation, and the recognition of the placebo effect, showing pain is subject to top-down influences.
3. The neuromatrix theory proposes pain arises from patterns of nerve impulses generated in widely distributed brain regions rather than a single pain center.
Acute pain management & preemptive analgesia (3)DR SHADAB KAMAL
This document discusses acute pain management and pre-emptive analgesia. It defines acute pain as pain caused by actual or potential tissue damage that is usually nociceptive in nature. Acute pain management primarily deals with patients recovering from surgery or acute medical conditions. Pre-emptive analgesia aims to prevent central neural sensitization by administering analgesics before a painful stimulus occurs, which can reduce both acute postoperative pain and the risk of chronic postsurgical pain. The document outlines various treatment approaches for acute pain management, including opioids, non-opioid analgesics, regional anesthetic techniques, and multimodal analgesia.
The document discusses the pathophysiology of pain. It defines pain and describes the three systems - sensory, motivational, and cognitive - that interact to produce the experience of pain. It categorizes pain into somatogenic, psychogenic, acute, and chronic types and discusses their characteristics. It also describes age-related differences in pain perception and the neuroanatomy of pain processing, including the roles of the afferent and efferent pathways and different areas of the central nervous system.
The document discusses various topics related to pain, including definitions, types, causes, symptoms, investigations, and treatments. It defines pain and differentiates it from nociception. It describes acute and chronic pain, as well as types including malignant and non-malignant pain. Physiological pain origins like cutaneous, somatic, and visceral pain are explained. Common and serious causes of pain in different body regions are listed. Investigations and various allopathic and alternative pain treatment methods are also outlined.
The document discusses pain management and analgesia. It outlines the consequences of untreated pain such as wasting, immune suppression, and increased risk of complications. It then covers the physiology of pain, types of pain responses, signs of pain, behavioral responses, and methods of pain assessment. Finally, it discusses various pharmacological agents for perioperative pain management including opioids, NSAIDs, local anesthetics, and other drugs, outlining their mechanisms of action, uses, and potential adverse effects.
Here are some key resources on pain and anxiety control in dentistry:
- Sturdvent - A leading manufacturer of dental equipment for pain and anxiety control.
- Ada's journal on anxiety and pain control - The American Dental Association's journal focused on non-pharmacological approaches.
- Journal on pain management by the American Society of Endodontists - Focuses on managing endodontic pain.
- Journal on pain control in dentistry - Focused specifically on controlling pain during various dental procedures.
- Pickard's manual of operative dentistry - A comprehensive textbook covering techniques for operative dentistry including pain control.
- Pain control in operative dentistry by Dr Ann Elrich - A
This chapter describes the neurological and neurosynaptic pathways for both acute and chronic pain. It also delineates the psychological differences between acute and chronic pain. Finally, it introduces the concept of the specific type of pain associated with a specific tissue type, which is useful in the diagnosis of pain problems. This chapter is the foundation for understanding all subsequent chapters on pain.
- Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It can be acute or chronic.
- Acute pain is sharp and short-lived, while chronic pain is intermittent or constant and lasts longer. Chronic pain is more difficult to treat.
- Pain has protective benefits like warning of injury and preventing further damage, but also has negative impacts. The physiology of pain involves receptors, pathways in the peripheral and central nervous systems, and neurotransmitters like glutamate and substance P. The gate control theory proposes mechanisms of pain modulation in the spinal cord and brain.
Current Update in the Management of Post-operative Neuraxial Opioid-induced P...asclepiuspdfs
This document summarizes the current pharmacological treatments available for managing opioid-induced pruritus caused by spinal opioids in postoperative patients. It discusses the mechanisms by which opioids induce pruritus, including activation of the itch center in the central nervous system and sensitization of peripheral nociceptors. The most useful drugs for treating or preventing pruritus are mu opioid receptor antagonists like naloxone, and mixed kappa opioid agonists/mu antagonists like nalbuphine and butorphanol. Other treatments with some efficacy include 5-HT3 serotonin receptor antagonists, D2 dopamine receptor antagonists, sub-anesthetic doses of propofol, and prophylaxis with mirtazapine
This document discusses pain pathways and treatments for pain. It begins by defining pain according to the IASP and describing the sensory and affective dimensions of pain. It then outlines the ascending pain pathway from peripheral receptors to the cortex. Several descending pain pathways are also described originating from the cortex, thalamus, and brainstem. Common craniofacial pain syndromes and their possible pathways are listed. Surgical and non-surgical treatment options for intractable pain are summarized, including neurostimulation, ablative procedures, and neuromodulation therapies.
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.
This document provides an overview of the physiology of pain. It discusses the definition of pain, the dual nature of fast and slow pain, pain stimuli and receptors, nerve pathways carrying pain signals to the brain, brain areas involved in pain perception, descending pain modulatory pathways, and neurochemicals involved in pain pathways. It summarizes different types of pain such as neuropathic pain and nociceptive pain. The gate control theory of pain and modifications to this theory are also briefly described.
The document discusses pain perception and transmission in the human body. It begins by defining pain and outlining the dual sensory and emotional nature of pain. It then describes how pain signals are transmitted from nociceptors to the spinal cord and brain through A and C nerve fibers. The signals travel through the spinothalamic tract to the thalamus and somatosensory cortex. Descending pathways from the brain can modulate pain perception. The gate control theory of pain is also explained. The document further discusses different types of pain and factors that influence pain experience.
This document discusses pain physiology, treatment options for pain, and common questions about pain. It explains that pain receptors detect potentially harmful stimuli and transmit pain messages to the spinal cord and brain. The brain then processes the pain and can send signals to reduce pain perception. Treatment options discussed include medications, mind-body practices, and self-care activities. Common questions addressed relate to aging and pain, assessing pain levels, medication risks and benefits, and the role of psychological factors in chronic pain.
Pain definition, pathway,analgesic pathway, types of painekta dwivedi
This document provides an overview of pain physiology, including definitions of pain, pain receptors and pathways, and theories of pain modulation. It discusses fast and slow pain fibers, pain transmission through the spinal cord and brain, and endogenous analgesic pathways. The gate control theory of pain is explained in detail. Different types of pain and assessment methods are outlined. Both pharmacological and non-pharmacological pain management approaches are summarized.
This study examined the relationship between falls and muscle strength, flexibility, and balance in 133 postmenopausal women with osteoporosis and 133 without osteoporosis. The researchers found that a significantly higher percentage of women with osteoporosis (51%) reported at least one fall in the previous year compared to women without osteoporosis (29%). Logistic regression analysis showed that lower trunk extension strength and the presence of osteoporosis were associated with an increased risk of falls. Specifically, greater trunk extension strength was associated with a lower risk of falls, while the presence of osteoporosis increased the risk of falls.
This document discusses trigeminal neuralgia (TN), a painful neurological condition that causes severe, sporadic facial pain. It begins with background on TN, describing its distinctive clinical history and pain patterns. The document then covers TN's anatomy and potential pathophysiologies, risk factors, characteristics, treatment options, complications, and prognosis over time. TN is caused by compression or irritation of the trigeminal nerve and presents as sudden, severe facial pain that may be triggered by everyday activities like chewing. While medication can provide initial relief, over time additional treatments like surgery may be needed to control breakthrough pain from this disabling condition.
This document describes a modern neuroscience approach for treating chronic spinal pain that combines pain neuroscience education with cognition-targeted motor control training. It discusses evidence that chronic spinal pain patients have abnormalities in brain structure and function, including decreased grey matter density, impaired motor control-related brain areas, and a sensitized brain due to central sensitization. The proposed approach has three phases: 1) Therapeutic pain neuroscience education to reconceptualize pain and explain central sensitization, 2) Cognition-targeted motor control training to address motor dysfunction, 3) Both 1) and 2) together to target peripheral and central mechanisms of chronic spinal pain.
Supportive and defensive communication climateshoranv
1. The document discusses Jack Gibb's theory of defensive and supportive communication behaviors that can alter a communication climate from negative and defensive to positive and open.
2. Gibb identified six defensive behaviors - evaluation, control, strategy, neutrality, superiority, and certainty - and six supportive behaviors - description, problem orientation, spontaneity, empathy, equality, and provisionalism.
3. Using supportive behaviors that confirm the other person, show concern for their feelings, and acknowledge uncertainty can help create a more positive communication climate where people feel free to open up.
O documento discute vários recursos utilizados na fisioterapia dermato-funcional, incluindo massoterapia, termoterapia, eletroterapia e atividade física. Detalha técnicas como massagem, crioterapia, hipertermoterapia, ultrassom, corrente galvânica, corrente russa, microcorrentes e laser, descrevendo suas indicações e contraindicações.
This document provides an analysis and recommendations for Mahindra's entry strategy into the dairy business in India. It begins with an overview of the dairy sector in India and opportunities for growth. It then outlines recommendations for Mahindra to enter through dairy extension services and developing small and large dairy farms. The document also analyzes the supply chain, potential products, customer segmentation, and provides a roadmap for Mahindra's entry and expansion over 5 years.
This short document does not provide enough context or details to generate a meaningful 3 sentence summary. It only contains the word "Flowers" with no other descriptions, events, people or identifiable elements that could be summarized at a high level.
The document lists and asks questions about various famous people from history, fiction, sports, and other domains. It asks the reader to consider what these people have in common, which ones had special powers, fulfilled dreams, helped humanity, won competitions, fought in wars, overcame problems, or created things for mankind. It then asks if the reader knows and considers other unnamed people to also be heroes, before posing questions about defining heroes, mentioning their characteristics and types of heroes.
Use Them or Lose Them: Old buildings with new purposesJonathanFoyle1
Annotated summary of the keynote lecture at the Resilient Heritage Conference, Peterborough 15 July 2011. Thinking out loud about how buildings must stay useful, and how we might achieve that most appropriately. Let the debate continue. More talks at www.built.org.uk
The document lists various products including biomagnetic pendants, diamond pendants, bracelets, water sticks, flasks, pens, suits, protection amulets, yantras, rudraksh beads, health products, kitchen tools, electronics and more. Each product listing includes the price in Rupees and number of codes included for that price.
Google is releasing their Mobile Algorithm Update on April 21, 2015. Learn 3 things you should know and 4 things you need to do to ensure your website is not affected!
Oh, It Ain't My Fault: Building Successful Marketing RelationshipsGeoff Coats
This document provides strategies for successfully managing creative projects that deliver results. It discusses defining the project goals and timeline, assembling the right internal and partner teams, aligning expectations by establishing a clear process and sharing assumptions, and managing the process by understanding what motivates creatives and reminding teams where they are. Great communication, trust between partners, flexibility, and investment in the project are keys to success.
This document contains plans and assignments for a Thanksgiving project. It lists team members and their roles, menus for the event including appetizers, salads, bread, turkey options and sides, desserts and drinks. It also includes schedules for tasks to prepare for the event on three dates, a materials list, ideas for family competitions during the event, and recipes for leftover turkey dishes.
Homer Novilla will lead others down the right path through guidance and inspiration in the Ateneo way. He finds strength in his faith in God and relies on his family for support. He aims to maintain balance in life between work, family, school, and friends while having passion for everything he does.
Neuropathic pain is caused by damage or dysfunction in the nervous system. It is initiated or caused by a primary lesion or dysfunction in either the peripheral or central nervous system. Common causes include diabetes, shingles, spinal cord injury, stroke, alcoholism and medications. This document discusses various types of neuropathic pain such as peripheral nerve damage and peripheral neuropathies. It also covers symptoms, diagnosis, examination tests and management options. The management of neuropathic pain focuses on treating underlying causes, reducing pain, improving function and quality of life. Pregabalin and gabapentin are considered first-line treatments and one study found that pregabalin was as effective as gabapentin for neuropathic pain associated with spinal cord injury.
This document discusses the pathway, physiology, and perception of pain. It begins with an introduction to pain and its significance as a warning signal. It then covers the history of theories about pain. The document defines pain and discusses its characteristics such as threshold, intensity, and localization. It classifies pain into acute and chronic types and looks at the components involved in pain perception including receptors, neural pathways, and sensory neurons. The document examines peripheral mechanisms of injury-induced pain and theories of pain such as the gate control theory. It also discusses visceral pain, referred pain, and tooth pain pathways.
oro-facial pain (other than neuralgias)Mammootty Ik
This document provides an overview of orofacial pain (OFP), including definitions, classifications, neural pathways, evaluation of patients, and treatment principles. OFP can be caused by diseases of the orofacial structures, musculoskeletal diseases, psychological factors, or referred pain from other sources. Evaluation of a patient with OFP involves taking a thorough history and performing a physical exam, with imaging and diagnostic nerve blocks used as needed to determine the cause. Classification systems organize OFP into physical and psychological categories to guide diagnosis and interdisciplinary treatment.
Pain is classified as nociceptive, neuropathic, or inflammatory based on its underlying mechanisms. Analgesics are commonly used in dentistry to manage pain and are classified as non-opioids such as NSAIDs or opioids. NSAIDs work by inhibiting cyclooxygenase enzymes to reduce prostaglandin production and provide anti-inflammatory, analgesic, and antipyretic effects, but can cause gastrointestinal, renal, and cardiovascular side effects.
The document discusses the physiology of pain. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It describes the dual nature of fast and slow pain mediated by different nerve fiber types. Stimuli that can cause pain and the receptors involved are discussed. The pathways that carry pain signals from receptors to the brain through the spinal cord and thalamus are summarized. Finally, it outlines the gate control theory of pain modulation by interactions between pain and touch fibers at the spinal cord.
The document discusses pharmacological treatments for phantom limb pain (PLP). It finds that while certain drugs can help aspects of PLP, no single treatment eliminates it. Opioids may help severe pain but have risks. Muscle relaxants can ease cramping. Psychological treatments like hypnosis and relaxation are also useful by reducing stress, a common PLP factor. The best approach may integrate pharmacological treatments with psychological ones to safely manage different PLP aspects.
Back Pain as a Central Sensitivity Spectrum DisorderPaul Coelho, MD
This document provides a narrative review of central sensitization as a potential pathophysiological mechanism underlying chronic low back pain. It describes central sensitization and the clinical signs associated with it, allowing for its recognition in patients with nonspecific low back pain. The review also discusses general treatment principles for chronic low back pain, with an emphasis on pharmacotherapy targeting central sensitization.
The document discusses pain and its management. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is subjective and involves physiological, emotional, and cognitive components. Pain assessment methods include WHATSUP, PQRST, and OLDCART. Pain management involves pharmacological approaches like opioids and non-opioids, surgical interventions, physical therapy, and complementary therapies like massage, acupuncture, and meditation. Nurses play a key role in comprehensive pain management.
This document provides an overview of pain pathways, physiology, and its application in pediatric dentistry. It begins with definitions of pain and discusses theories of pain such as the intensity theory, specificity theory, and gate control theory. It then covers components of the pain system including neurons, central and peripheral nervous systems, and classification of orofacial pain. The document aims to provide understanding of basic pain mechanisms and physiology to effectively manage pediatric patients experiencing pain.
This document provides information on pain, including its definition, functions, categories, and transmission and perception in the nervous system. It discusses how pain is classified based on its inferred pathophysiology into nociceptive and neuropathic pain. It also summarizes factors that lower and raise pain thresholds, and outlines the World Health Organization's step ladder approach to pain management. Major topics covered include gate control theory, types of somatic sensations, targets of pain treatment, and drugs used for neuropathic pain such as NSAIDs, opioids, antidepressants, and anticonvulsants.
This document summarizes several chronic pain conditions and their treatments. It discusses myofascial pain, intercostal neuralgia, postherpetic neuralgia, complex regional pain syndrome types I and II, cancer pain, and various procedures to treat them. These procedures include trigger point injections, transcutaneous electrical nerve stimulation, spinal cord stimulation, peripheral nerve stimulation, neurolytic blocks, sympathetic nerve blocks, regional anesthesia techniques, and drug therapies. The document provides details on anatomy, signs and symptoms, and techniques for specific procedures to manage chronic pain conditions.
Tender points are areas of the body that experience different types of pain when pressure is applied to them.
A Trigger Point (TrP) is a hyperirritable spot, a palpable nodule in the taut bands of the skeletal muscles' fascia.
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
INTRODUCTION
HISTORY
EPIDEMIOLOGY
DEFINITIONS OF PAIN
BENEFITS OF PAIN
NOCICEPTION
PAIN RECEPTORS
THEORIES OF PAIN
CHARACTERISTICS OF PAIN
PAIN PATHWAY
MECHANISM OF PAIN
PAIN ASSESSMENT
APPLIED ASPECTS
CONCLUSION
REFERENCES
Myofascial pain is a common condition caused by trigger points in muscles that produce pain and motor and autonomic symptoms. Trigger points are focal areas of tenderness caused by hypercontracted muscle tissue. Myofascial pain syndrome is characterized by localized pain that differs from fibromyalgia which causes widespread pain. Trigger points are classified as active or latent based on whether they cause spontaneous pain. Diagnosis involves palpation to identify taut bands and tender spots. Treatment includes non-invasive techniques like stretching, massage, and dry needling as well as invasive techniques like injections.
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3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
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1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Myofascial trigger points peripheral or central phenomenon-
1. Curr Rheumatol Rep (2014) 16:395
DOI 10.1007/s11926-013-0395-2
CHRONIC PAIN (R STAUD, SECTION EDITOR)
Myofascial Trigger Points: Peripheral
or Central Phenomenon?
César Fernández-de-las-Peñas & Jan Dommerholt
Published online: 22 November 2013
# Springer Science+Business Media New York 2013
Abstract Trigger points (TrP) are hyperirritable spots in a
taut band of a skeletal muscle, which usually have referred
pain. There is controversy over whether TrP are a peripheral or
central nervous system phenomenon. Referred pain, the most
characteristic sign of TrP, is a central phenomenon initiated
and activated by peripheral sensitization, whereby the peripheral nociceptive input from the muscle can sensitize dorsal
horn neurons that were previously silent. TrP are a peripheral
source of nociception, and act as ongoing nociceptive stimuli
contributing to pain propagation and widespread pain. Several
studies support the hypothesis that TrP can induce central
sensitization, and appropriate TrP treatment reduces central
sensitization. In contrast, preliminary evidence suggests that
central sensitization can also promote TrP activity, although
further studies are needed. Proper TrP management may prevent and reverse the development of pain propagation in
chronic pain conditions, because inactivation of TrP attenuates
central sensitization.
This article is part of the Topical Collection on Chronic Pain
Introduction
C. Fernández-de-las-Peñas
Department Physical Therapy, Occupational Therapy, Rehabilitation
and Physical Medicine, Universidad Rey Juan Carlos, Alcorcón,
Madrid, Spain
C. Fernández-de-las-Peñas
Esthesiology Laboratory of Universidad Rey Juan Carlos, Alcorcón,
Madrid, Spain
C. Fernández-de-las-Peñas
Cátedra de Investigación y Docencia en Fisioterapia: Terapia Manual
y Punción Seca, Universidad Rey Juan Carlos, Alcorcón, Madrid,
Spain
J. Dommerholt
Myopain Seminars, LLC, Bethesda Physiocare, Inc, Bethesda, MD,
USA
J. Dommerholt
Universidad CEU Cardenal Herrera, Valencia, Spain
J. Dommerholt
Shenandoah University, Winchester, VA, USA
C. Fernández-de-las-Peñas (*)
Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos,
Avenida de Atenas s/n, 28922 Alcorcón, Madrid, Spain
e-mail: cesar.fernandez@urjc.es
Keywords Trigger points . Referred pain . Sensitization .
Central . Peripheral . Myofascial . Nociception
Myofascial trigger points (TrP) are one of the most overlooked
and ignored causes of musculoskeletal pain. There is evidence
suggesting that TrP are a common primary dysfunction and
not necessarily secondary to other diagnoses [1]. In other
words, TrP may occur in the absence of any underlying
medical condition and can constitute an independent cause
of pain. TrP can, however, also be co-morbid with a variety of
medical musculoskeletal conditions, including osteoarthritis
of the hip or knee [2], or with visceral conditions, for example
endometriosis [3], interstitial cystitis [4], irritable bowel syndrome, dysmenorrhea, or prostatitis [5].
The most commonly accepted definition describes a TrP as
a hyperirritable spot in a taut band of a skeletal muscle, which
is painful on compression, stretch, overload, or contraction of
the muscle and usually has a distinct referred pain pattern [6].
Clinically, we can distinguish active and latent TrP. The local
and referred pain from active TrP reproduces symptoms suffered by patients, who identify the pain as their usual or
familiar pain. There is evidence that the local and referred pain
from active TrP reproduces the sensory symptoms of individuals with idiopathic neck pain [7], lateral epicondylalgia [8],
chronic tension-type headache [9], shoulder pain [10, 11], and
2. 395, Page 2 of 6
temporomandibular pain [12]. In contrast, the local and referred pain from latent TrP may not reproduce any symptom
familiar or usual to the patient [6].
Although latent TrP do not induce spontaneous pain,
they can provoke motor dysfunction, e.g. muscle weakness, inhibition, increased motor irritability [13], muscle
cramps [14], and altered motor recruitment [15]. During
the past decade, an increasing number of researchers have
shown an interest in the etiology and clinical relevance of
latent TrP [16••].
Development or activation of TrP can result from a variety
of factors, including repetitive muscle overuse, acute muscle
overload, repetitive minor muscle trauma, psychological
stress, and visceral disorders [17]. TrP are located within
discrete bands of contractured muscle fibers called taut bands.
A taut band signifies a contracture arising endogenously within a limited number of muscle fibers, but not involving the
entire muscle [6]. Studies have observed that taut bands have
higher stiffness [18], reduced vibration amplitude [19], higher
peak systolic velocities, and negative diastolic velocities [20]
compared with normal muscle sites. Although different theories have been proposed, the integrated hypothesis is the most
accepted model for explaining the pathophysiology of muscle
TrP [21•]. In summary, the integrated hypothesis proposes that
abnormal depolarization of the post-junctional membrane of
motor endplates causes a localized hypoxic energy crisis
associated with sensory and autonomic reflex arcs that are
sustained by complex sensitization mechanisms. The presence
of spontaneous electrical activity or endplate noise, and the
clinical evidence that treating TrP eliminates or significantly
reduces this endplate noise, support the notion that TrP are
located in close proximity to dysfunctional motor endplates
[22]. A recent study reported that TrP in the upper trapezius
muscle are located in well-defined areas proximal to innervation muscle zones [23]. Although current evidence supports
the hypothesis that TrP are associated with dysfunctional
motor endplates, the function of muscle spindles in the etiology of TrP has been also investigated [24–26].
The integrated hypothesis postulates that the origin of TrP
is a primary dysfunction of the motor endplate. A more recent
hypothesis suggests that TrP are caused by a nociceptioninduced central nervous system disorder, which is centrally
maintained by α-motoneuron plateau depolarization, but experimental evidence for this hypothesis is lacking [27].
Recently, several researchers have investigated a possible
relationship between TrP and sensitization mechanisms
[28••]. TrP may be a cause of central sensitization, but it is
also conceivable that TrP are the result of central sensitization;
in other words, are TrP a peripheral or a central phenomenon?
This paper will discuss different sensory aspects of TrP,
whereby both peripheral and central sensitization mechanisms
are involved simultaneously, and briefly address clinical
implications.
Curr Rheumatol Rep (2014) 16:395
Muscle Referred Pain: Peripheral or Central
Phenomenon?
One of the characteristic signs of TrP is the presence of referred
pain. Pain felt at the source of pain is termed “local pain” or
“primary pain,” whereas pain felt in a region away from the
source of pain is termed “referred pain.” Referred pain can be
perceived in any region of the body, but the size of the referred
pain area is variable and at least partially affected by paininduced changes to central somatosensory maps. Because the
intensity of referred pain and the size of the referred pain area
are positively correlated with central nervous system excitability, it is now generally assumed that muscle referred pain is a
central sensitization process mediated by a peripheral sensitization phenomenon, with additional sympathetic activity facilitation and dysfunctional descending pain inhibition [29, 30].
Among the different theories explaining the neurophysiology of referred pain, the central hyper-excitability theory
explains the principal characteristics of referred pain in most
detail. According to this theory, referred pain occurs at the
dorsal horn level and is the result of activation, by means of
sensitization mechanisms, of quiescent axonal connections
between affective nerve fibers’ dorsal horn neurons [1].
Hoheisel et al. reported that new receptive fields emerged
within minutes after experience of noxious stimuli [31],
explaining the delay between the noxious input and development of referred pain [32]. In clinical practice referred pain
appears within seconds of stimulation of a TrP, suggesting that
induction of these axonal changes is a rapid process. TrP are
more effective than non-TrP regions at inducing neuroplastic
changes in the dorsal horn neurons [33].
These findings support the hypothesis that referred pain
elicited by TrP is a central phenomenon initiated, activated,
and maintained by peripheral sensitization. Peripheral nociceptive input can sensitize previously silent dorsal horn neurons. Because anesthetization of the referred pain area reduces
pain, it would seem that peripheral processes contribute to
referred pain [34].
However, it is also clear that central sensitization processes
are involved in the development of spreading pain, because
larger referred pain areas in patients with chronic pain are a
consequence of higher central neural plasticity [35]. Maintenance of referred pain is dependent on ongoing nociceptive
input from the site of primary muscle pain [29]. There is
currently insufficient data to determine which sensitization
mechanism, peripheral or central, is more relevant to the
development of referred pain.
Trigger Points: A Peripheral Source of Nociception
Peripheral sensitization is described as a reduction in the pain
threshold and an increase in responsiveness of the peripheral
3. Curr Rheumatol Rep (2014) 16:395
nociceptors. Muscle pain is associated with the activation of
muscular nociceptors by a variety of endogenous substances,
including neuropeptides and inflammatory mediators [1].
Studies conducted by Shah et al. revealed that the concentrations of bradykinin (BK), calcitonin gene-related peptide
(CGRP), substance P, tumor necrosis factor-α (TNF-α), interleukins 1β, IL-6, and IL-8, serotonin (5-HT), and norepinephrine were significantly higher at active TrP than at latent TrP or
non-TrP points [36]. Interestingly, concentrations of the same
biochemical and algogenic substances in a pain-free area of
the gastrocnemius muscle were also higher for subjects with
active TrP in the upper trapezius muscle compared with subjects with latent TrP or non-TrP points [37]. More recently,
Hsieh et al. confirmed the presence of multiple biochemical
substances in the immediate proximity of TrP [38••]. Both the
studies by Shah et al. [36, 37] and Hsieh et al. [38••] provided
evidence that therapeutic intervention with dry needling could
modulate and normalize the chemical environment of TrP,
supporting the theory that TrP may be a source of peripheral
nociceptive input.
Li et al. observed nociceptive (hyperalgesia) and nonnociceptive (allodynia) hypersensitivity at TrP, suggesting that
TrP sensitize nociceptive and non-nociceptive nerve endings
[39]. Wang et al. reported that blocking large-diameter myelinated muscle afferents increased pressure pain and referred
pain thresholds at TrP, but not at non-TrP regions, suggesting
that non-nociceptive large-diameter myelinated muscle afferents are also involved in TrP pain [40]. These studies establish
the presence of nociceptive pain hypersensitivity at TrP and
confirm that TrP are a focus of peripheral sensitization.
Myofascial TrP can act as ongoing nociceptive stimuli
contributing to spatial pain propagation and widespread pain,
as confirmed by a study in which painful stimulation of latent
TrP in asymptomatic subjects induced early occurrence of a
locally enlarged area of pressure hyperalgesia and central
sensitization [41].
Trigger Points can Induce Central Sensitization
Emerging research suggests a physiological link between the
clinical manifestations of TrP, e.g. hyperalgesia, allodynia,
and referred pain, and central sensitization, although the causal mechanisms are still unclear. Mense suggested that, because
TrP constitute a continued peripheral nociceptive afferent
barrage into the central nervous system, the presence of multiple TrP in the same or different muscles or the presence of
TrP for prolonged periods of time can sensitize spinal cord
neurons and supra-spinal structures [42].
A relationship between active TrP and central sensitization
has been suggested for many years, but it was not until the past
decade that neuro-physiological studies were initiated. Kuan
et al. observed that spinal cord connections of TrP were more
Page 3 of 6, 395
effective than non-TrP tissue at inducing neuroplastic changes
in the dorsal horn neurons, and were connected to a greater
number of small sensory or nociceptive neurons [33]. Xu et al.
reported that painful stimulation of latent TrP induced central
sensitization in healthy subjects, because stimulation of TrP
increased pressure hypersensitivity of extra-segmental tissues
[43]. A few studies observed that stimulation of TrP induced
enhanced activity of brain areas including the primary and
secondary somatosensory cortex, the inferior parietal cortex,
and the mid and anterior insula [44, 45], supporting the
hypothesis that TrP can induce central sensitization.
TrP are also a focus of peripheral noxious sensitization, as
illustrated by Fernández-de-las-Peñas et al., who formulated a
pain model applied to tension-type headache. Peripheral sensitization of muscle nociceptors and central sensitization both
seem to be linked to active TrP located in muscles innervated
by the upper cervical nerve roots and the trigeminal nerve. TrP
may be responsible for peripheral nociception and produce a
continuous afferent barrage into the trigeminal nerve nucleus
caudalis, hence sensitizing the central nervous system [46].
Further support for the hypothesis that TrP may induce central
sensitization can be derived from the observation that proper
management of TrP can reduce central sensitization. There is
evidence that central sensitization is a reversible process in
individuals with TrP [35], although traditionally central sensitization has been believed an irreversible process, at least in
animals [47]. Injections into TrP of neck muscles produced
rapid relief of palpable scalp and facial tenderness and associated symptoms of migraine [48]. Anesthetic injections into
active TrP significantly reduced mechanical hyperalgesia,
allodynia, and referred pain for individuals with migraine
[49], fibromyalgia [50], and whiplash [51].
The cause of the rapid decrease in local and referred pain
associated with TrP therapy, observed in clinical practice, is
not fully understood. The resolution of TrP-associated referred
pain is related to the decrease of nociceptive input to dorsal
horn neurons of the spinal cord, and to interruption of the
spread of pain and central sensitization. The reversal of referred pain is fast, suggesting that central sensitization can
indeed be reversed with proper treatment. A recent study
supported the hypothesis that altered pain processing seems
to be driven by peripheral noxious stimuli. The researchers
described normalization of widespread pressure-pain
hyperalgesia after successful hip replacement in subjects with
symptomatic hip osteoarthritis [52]. Several factors affect
central sensitization associated with TrP, including descending
inhibitory pathways and sympathetic or neuropathic activity.
Central Sensitization can Promote Trigger Point Activity
Although there is evidence that TrP can initiate central sensitization, there is also some preliminary evidence that central
4. 395, Page 4 of 6
sensitization can promote TrP activity. It is known that a
sensitized central nervous system may modulate referred muscle pain. For example, infusions of the N-methyl-D-aspartate
(NMDA) antagonist ketamine reduced referred pain areas in
subjects with fibromyalgia [53]. In addition, an increased
degree of central sensitization is associated with larger referred pain areas from TrP [1, 9, 29].
The only study suggesting that TrP can result from central
sensitization was conducted by Srbely et al. [54], who hypothesized that pain arising from TrP may be caused by neurogenic
mechanisms secondary to central sensitization. They postulated that central sensitization may increase TrP sensitivity in
segmentally related muscles; however, the study did not establish a cause-and-effect relationship [54]. If central sensitization could cause TrP, it would be reasonable to assume that
TrP would not be present in healthy, pain-free subjects where
central sensitization mechanisms are not present. There are,
however, several studies revealing that asymptomatic healthy
subjects also have TrP—because the subjects are pain free,
these would be classified as latent TrP, [2, 3, 7–15, 16••, 23,
24, 40, 41, 43]. Latent TrP are not spontaneously painful, but
they do provide nociceptive barrage into the dorsal horn
[13–15, 16••, 24, 40, 41, 43].
Although there is no evidence supporting the hypothesis
that TrP are a result of central sensitization, in clinical practice
individuals with higher levels of central sensitization present
with multiple TrP.
Implications for Clinical Practice
Current data supports the hypothesis that TrP can affect the
development of central sensitization. Because muscle TrP are
common in many chronic pain conditions and they initiate,
activate, and maintain sensitization of central pathways, it is
important to realize that untreated TrP can cause chronic or
persistent pain. Therefore, TrP should be treated as soon and
as effectively as possible to avoid development of persistent
pain. Proper management of TrP may prevent and reverse the
development of spatial pain propagation in chronic pain conditions. Inactivation of TrP is associated with attenuation of
central sensitization [49–51] and induction of spinal inhibition
[55, 56]. Determining the proper treatment approach for each
individual patient with chronic or persistent pain is challenging for clinicians, because patients will probably have different clinical presentations. In developing an effective management plan, the manifestations of both peripheral and central
sensitization mechanisms of a particular condition or clinical
presentation must be included in the decision tree. In other
words, clinical management of patients with central sensitization needs to extend beyond tissue-based pathology and incorporate strategies directed at normalizing or reducing central
nervous system sensitivity [57].
Curr Rheumatol Rep (2014) 16:395
The treatment plan should include two main components. First, peripheral and central nervous system sensitivity must be targeted by means of appropriate interventions. Second, the descending inhibitory systems must be
activated [58]. Inactivating TrP and addressing their perpetuating and promoting factors has an important function
in achieving these objectives, because removing the peripheral nociceptive input from TrP will modulate the
patient’s central sensitivity.
Clinically, when a patient presents with a pain problem
mediated by predominantly peripheral sensitization mechanisms, functional activity and early and appropriate treatment of the noxious inputs should be encouraged. This
may involve inactivating TrP, and mobilizing joints and
nerves. For a patient with a more persistent condition
mediated by predominantly central sensitization mechanisms, a multimodal therapy program is the preferred
approach, which may include pharmacological and medical management, physical therapy, and cognitive behavioral or psychodynamic therapy. Depending on the chronicity of the disorder and the associated disability, patients
should receive pain neuroscience education addressing the
neurobiology of pain and pain mechanisms, fear, anxiety,
and other psychosocial variables [59]. Patients need to
develop different strategies for optimizing normal functional movement and to undertake active and specific or
more global exercises, including aerobic exercise.
Conclusions
To determine whether muscle TrP are a peripheral or
central phenomenon, multiple lines of research must be
considered. Available data supports the hypothesis that
TrP are a persistent peripheral source of nociception contributing to pain propagation and widespread pain. The
clinical finding that inactivating TrP attenuates central
sensitization further supports the hypothesis that TrP are
a primarily peripheral phenomenon. As research in this
field continues to expand, it is conceivable that central
phenomena will be found to contribute to the development of TrP. However, experimental evidence is currently
sparse.
Compliance with Ethics Guidelines
Conflict of Interest César Fernández-de-las-Peñas and Jan Dommerholt
declare that they have no conflict of interest.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
5. Curr Rheumatol Rep (2014) 16:395
References
Papers of particular interest, published recently, have been
highlighted as:
• Of importance
•• Of major importance
Page 5 of 6, 395
19.
20.
21.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Mense S, Gerwin RD, editors. Muscle pain: understanding the
mechanisms. Berlin: Springer-Verlag; 2010.
Bajaj P, Bajaj P, Graven-Nielsen T, Arendt-Nielsen L. Trigger
points in patients with lower limb osteoarthritis. J Musculoskelet
Pain. 2001;9(3):17–33.
Jarrell J. Endometriosis and abdominal myofascial pain in adults
and adolescents. Curr Pain Headache Rep. 2011;15:368–76.
Weiss JM. Pelvic floor myofascial trigger points: manual therapy
for interstitial cystitis and the urgency–frequency syndrome. J Urol.
2001;166:2226–31.
Doggweiler-Wiygul R. Urologic myofascial pain syndromes. Curr
Pain Headache Rep. 2004;8:445–51.
Simons DG, Travell JG, Simons LS. Myofascial pain and dysfunction: the trigger point manual, vol. 1. Philadelphia: Lippincott
William & Wilkins; 1999.
Fernández-de-las-Peñas C, Alonso-Blanco C, Miangolarra JC.
Myofascial trigger points in subjects presenting with mechanical
neck pain: a blinded, controlled study. Man Ther. 2007;12:29–33.
Fernández-Carnero J, Fernández-de-las-Peñas C, de-la-LlaveRincón AI, Ge HY, Arendt-Nielsen L. Prevalence of and referred
pain from myofascial trigger points in the forearm muscles in
patients with lateral epicondylalgia. Clin J Pain. 2007;23:353–60.
Fernández-de-las-Peñas C, Schoenen J. Chronic tension type headache: what’s new? Curr Opin Neurol. 2009;22:254–61.
Ge HY, Fernández-de-las-Peñas C, Madeleine P, Arendt-Nielsen L.
Topographical mapping and mechanical pain sensitivity of
myofascial trigger points in the infraspinatus muscle. Eur J Pain.
2008;12:859–65.
Bron C, Dommerholt J, Stegenga B, Wensing M, Oostendorp RA.
High prevalence of shoulder girdle muscles with myofascial trigger
points in patients with shoulder pain. BMC Musculoskelet Disord.
2011;12:139.
Fernández-de-las-Peñas C, Galán-del-Río F, Alonso-Blanco C,
Jiménez-García R, Arendt-Nielsen L, Svensson P. Referred pain
from muscle trigger points in the masticatory and neck-shoulder
musculature in women with temporomandibular disorders. J Pain.
2010;11:1295–304.
Ibarra JM, Ge HY, Wang C, Martínez Vizcaíno V, Graven-Nielsen
T, Arendt-Nielsen L. Latent myofascial trigger points are associated
with an increased antagonistic muscle activity during agonist muscle contraction. J Pain. 2011;12:1282–8.
Ge HY, Zhang Y, Boudreau S, Yue SW, Arendt-Nielsen L.
Induction of muscle cramps by nociceptive stimulation of latent
myofascial trigger points. Exp Brain Res. 2008;187:623–9.
Lucas KR, Rich PA, Polus BI. Muscle activation patterns in the
scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points. Clin Biomech.
2010;25:765–70.
•• Ge HY, Arendt-Nielsen L. Latent myofascial trigger points. Curr
Pain Head Rep. 2011;15:386–92. An updated article supporting the
clinical relevance of latent trigger points.
Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons’
integrated hypothesis of trigger point formation. Curr Pain
Headache Rep. 2004;8:468–75.
Chen Q, Bensamoun S, Basford JR, et al. Identification and quantification of myofascial taut bands with magnetic resonance
elastography. Arch Phys Med Rehabil. 2007;88:1658–61.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
Sikdar S, Shah JP, Gilliams E, et al. Novel applications of ultrasound technology to visualize and characterize myofascial trigger
points and surrounding soft tissue. Arch Phys Med Rehabil.
2009;90:1829–38.
Sikdar S, Ortiz R, Gebreab T, Gerber LH, Shah JP. Understanding
the vascular environment of myofascial trigger points using ultrasonic imaging and computational modeling. Conf Proc IEEE Eng
Med Biol Soc. 2010;1:5302–5.
• Bron C, Dommertholt J. Etiology of myofascial trigger points.
Curr Pain Headache Rep. 2012;16:439–44. An article updating the
etiology of muscle trigger points.
Ge HY, Fernández-de-las-Peñas C, Yue SW. Myofascial trigger
points: spontaneous electrical activity and its consequences for pain
induction and propagation. Chin Med. 2011;6:13.
Barbero M, Cescon C, Tettamanti A, Leggero V, Macmillan F,
Coutts F, et al. Myofascial trigger points and innervation zone
locations in upper trapezius muscles. BMC Musculoskelet Disord.
2013;14:179.
Ge HY, Serrao M, Andersen OK, Graven-Nielsen T, ArendtNielsen L. Increased H-reflex response induced by intramuscular
electrical stimulation of latent myofascial trigger points. Acupunct
Med. 2009;27:150–4.
Partanen JV. End plate spikes in the human electromyogram.
Revision of the fusimotor theory. J Physiol Paris. 1999;93:155–66.
Partanen JV, Ojala TA, Arokoski PA. Myofascial syndrome and
pain: a neurophysiological approach. Pathophysiology. 2010;17:
19–28.
Hocking MJL. Exploring the central modulation hypothesis: do
ancient memory mechanisms underlie the patho-physiology of
trigger points? Curr Pain Headache Rep. 2013;17:347.
•• Dommertholt J. Dry needling: peripheral and central considerations. J Manual Manipulative Ther. 2011;19:223–37. An article
suggesting a relationship between sensitization and trigger points.
Arendt-Nielsen L, Svensson P. Referred muscle pain: basic and
clinical findings. Clin J Pain. 2001;17:11–9.
Arendt-Nielsen L, Sluka KA, Nie HL. Experimental muscle pain
impairs descending inhibition. Pain. 2008;40:465–71.
Hoheisel U, Mense S, Simons DG, Yu XM. Appearance of new
receptive fields in rat dorsal horn neurons following noxious stimulation of skeletal muscle: a model for referral of muscle pain?
Neurosci Lett. 1993;153:9–12.
Graven-Nielsen T, Arendt-Nielsen L, Svensson P, Jensen TS.
Quantification of local and referred muscle pain in humans after
sequential intra-muscular injections of hypertonic saline. Pain.
1997;69:111–7.
Kuan TS, Hong CZ, Chen JT, Chen SM, Chien CH. The spinal cord
connections of the myofascial trigger spots. Eur J Pain. 2007;11:
624–34.
Rubin TK, Gandevia SC, Henderson LA, Macefield VG. Effects of
intramuscular anesthesia on the expression of primary and referred
pain induced by intramuscular injection of hypertonic saline. J Pain.
2009;10:829–35.
Arendt-Nielsen L, Laursen RJ, Drewes AM. Referred pain as an
indicator for neural plasticity. Prog Brain Res. 2000;129:343–56.
Shah JP, Phillips TM, Danoff JV, Gerber LH. An in-vivo microanalytical technique for measuring the local biochemical milieu of
human skeletal muscle. J Appl Physiol. 2005;99:1977–84.
Shah JP, Danoff JV, Desai MJ, Parikh S, Nakamura LY,
Phillips TM, et al. Biochemicals associated with pain and
inflammation are elevated in sites near to and remote from
active myofascial trigger points. Arch Phys Med Rehabil.
2008;89:16–23.
•• Hsieh XL, Yang SA, Yang CC, Chou LW. Dry needling at
myofascial trigger spots of rabbit skeletal muscles modulates the
biochemicals associated with pain, inflammation, and hypoxia.
Evid Based Complement Alternat Med. 2012;2012:342165. An
6. 395, Page 6 of 6
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
article confirming that trigger points are a peripheral source of
nociception.
Li LT, Ge HY, Yue SW, Arendt-Nielsen L. Nociceptive and nonnociceptive hypersensitivity at latent myofascial trigger points. Clin
J Pain. 2009;25:132–7.
Wang YH, Ding X, Zhang Y, et al. Ischemic compression block
attenuates mechanical hyperalgesia evoked from latent myofascial
trigger point. Exp Brain Res. 2010;202:265–7.
Wang C, Ge HY, Ibarra JM, Yue SW, Madeleine P, Arendt-Nielsen
L. Spatial pain propagation over time following painful glutamate
activation of latent myofascial trigger points in humans. J Pain.
2012;13:537–45.
Mense S. Referral of muscle pain. APS J. 1994;3:1–9.
Xu YM, Ge HY, Arendt-Nielsen L. Sustained nociceptive mechanical stimulation of latent myofascial trigger point induces central
sensitization in healthy subjects. J Pain. 2010;11:1348–55.
Niddam DM, Chan RC, Lee SH, Yeh TC, Hsieh J. Central representation of hyperalgesia from myofascial trigger point.
Neuroimage. 2008;39:1299–306.
Niddam DM. Brain manifestation and modulation of pain from
myofascial trigger points. Curr Pain Headache Rep. 2009;13:370–5.
Fernández-de-las-Peñas C, Cuadrado ML, Arendt-Nielsen L,
Simons DG, Pareja JA. Myofascial trigger points and sensitization:
an updated pain model for tension type headache. Cephalalgia.
2007;27:383–93.
Sluka KA, Kalra A, Moore SA. Unilateral intramuscular injections
of acidic saline produce a bilateral, long-lasting hyperalgesia.
Muscle Nerve. 2001;24:37–46.
Mellick GA, Mellick LB. Regional head and face pain relief following lower cervical intramuscular anesthetic injection. Headache.
2003;43:1109–11.
Giamberardino MA, Tafuri E, Savini A, et al. Contribution of
myofascial trigger points to migraine symptoms. J Pain. 2007;8:
869–78.
Affaitati G, Costantini R, Fabrizio A, Lapenna D, Tafuri E,
Curr Rheumatol Rep (2014) 16:395
Giamberardino M. Effects of treatment of peripheral pain generators in fibromyalgia patients. Eur J Pain. 2011;15:61–9.
51. Freeman MD, Nystrom A, Centeno C. Chronic whiplash and
central sensitization; an evaluation of the role of a myofascial
trigger points in pain modulation. J Brachial Plex Peripher Nerve
Inj. 2009;4:2.
52. Aranda-Villalobos P, Fernández-de-Las-Peñas C, NavarroEspigares JL, Hernández-Torres E, Villalobos M, Arendt-Nielsen
L, et al. Normalization of widespread pressure pain hypersensitivity
after total hip replacement in patients with hip osteoarthritis is
associated with clinical and functional improvements. Arthritis
Rheum. 2013;65:1262–70.
53. Graven-Nielsen T, Aspegren-Kendall S, Henriksson KG, et al.
Ketamine attenuates experimental referred muscle pain and temporal summation in fibromyalgia patients. Pain. 2000;85:483–91.
54. Srbely JZ, Dickey JP, Bent LR, Lee D, Lowerison M. Capsaicininduced central sensitization evokes segmental increases in trigger
point sensitivity in humans. J Pain. 2010;11:636–43.
55. Srbely JZ, Dickey JP, Lowerison M, Edwards AM, Nolet PS, Wong
LL. Stimulation of myofascial trigger points with ultrasound induces segmental antinociceptive effects: a randomized controlled
study. Pain. 2008;139:260–6.
56. Srbely JZ, Dickey JP, Lee D, Lowerison M. Dry needle stimulation
of myofascial trigger points evokes segmental anti-nociceptive
effects. J Rehabil Med. 2010;42:463–8.
57. Nijs J, Van Houdenhove B, Oostendorp RA. Recognition of central
sensitization in patients with musculoskeletal pain: application of
pain neurophysiology in manual therapy practice. Man Ther.
2010;15:135–41.
58. Nijs J, Meeus M, Van Oosterwijck J, Roussel N, De Kooning M,
Ickmans K, et al. Treatment of central sensitization in patients with
'unexplained' chronic pain: what options do we have? Expert Opin
Pharmacother. 2011;12:1087–98.
59. Puentedura EL, Louw A. A neuroscience approach to managing
athletes with low back pain. Phys Ther Sports. 2012;13:123–33.