1) The document discusses pain physiology including types of pain, pain pathways, and the brain's analgesic system.
2) It describes how pain is carried via different nerve fibers and pathways to the dorsal horn, thalamus, and sensory cortex.
3) It explains referred pain and how visceral pain can be felt in distant areas of the body according to dermatomal rules due to convergence in the central nervous system.
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.
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 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.
1) Pain involves complex neurophysiological processes including transduction, transmission, modulation, and perception of pain signals in the peripheral and central nervous systems.
2) Nociceptive fibers detect and transmit noxious stimuli from the periphery to the spinal cord. Transmission involves both myelinated Aδ fibers and unmyelinated C fibers.
3) Modulation of pain occurs both peripherally by inflammatory mediators and centrally through descending inhibitory pathways and neurotransmitters like opioids. Central sensitization in the spinal cord dorsal horn can lead to hyperalgesia and allodynia.
This document provides an overview of pain, including its definition, types, and pathway in the human body. It discusses how pain is sensed by nociceptors and transmitted through the nervous system to be perceived in the brain. Acute and chronic pain are compared, and the mechanisms of nociceptive and neuropathic pain explained. Somatic, visceral, referred, somatogenic, and psychogenic pain are defined. The neuroanatomy and physiology of pain processing through transduction, transmission, modulation, and perception are outlined in detail.
The document discusses pain, including its definition, types, perception and pathways. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It classifies pain into physiological (nociceptive), pathological (neuropathic), and psychogenic types based on its mechanism or cause. The neural pathways for pain transmission, including the neospinothalamic and paleospinothalamic tracts, are described. The concepts of referred pain and the endogenous analgesia system, including the gate control theory, are also summarized.
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.
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 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.
1) Pain involves complex neurophysiological processes including transduction, transmission, modulation, and perception of pain signals in the peripheral and central nervous systems.
2) Nociceptive fibers detect and transmit noxious stimuli from the periphery to the spinal cord. Transmission involves both myelinated Aδ fibers and unmyelinated C fibers.
3) Modulation of pain occurs both peripherally by inflammatory mediators and centrally through descending inhibitory pathways and neurotransmitters like opioids. Central sensitization in the spinal cord dorsal horn can lead to hyperalgesia and allodynia.
This document provides an overview of pain, including its definition, types, and pathway in the human body. It discusses how pain is sensed by nociceptors and transmitted through the nervous system to be perceived in the brain. Acute and chronic pain are compared, and the mechanisms of nociceptive and neuropathic pain explained. Somatic, visceral, referred, somatogenic, and psychogenic pain are defined. The neuroanatomy and physiology of pain processing through transduction, transmission, modulation, and perception are outlined in detail.
The document discusses pain, including its definition, types, perception and pathways. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It classifies pain into physiological (nociceptive), pathological (neuropathic), and psychogenic types based on its mechanism or cause. The neural pathways for pain transmission, including the neospinothalamic and paleospinothalamic tracts, are described. The concepts of referred pain and the endogenous analgesia system, including the gate control theory, are also summarized.
This document discusses reflex activity and the physiology of muscles and their receptors. It begins by defining a motor unit and describing the various muscle sensors, including the muscle spindle, Golgi tendon organ, and Pacinian corpuscle. It then focuses on the structure and function of the muscle spindle, its sensory and motor innervation, and its roles in proprioception and the stretch reflex. Finally, it briefly outlines muscle tone, classifications of reflexes, and preparations used to study reflexes experimentally.
This document discusses receptors and neurons that detect sensory information. It begins by defining perception and describing how sensory information is transmitted from receptors to the central nervous system. It then categorizes the different sensory modalities like touch, pain, temperature, and proprioception. The document goes on to describe the different types of sensory receptors, including their locations, the stimuli they detect, and whether they adapt rapidly or slowly. It provides examples of specific receptors like Meissner corpuscles, Pacinian corpuscles, and thermoreceptors. In closing, it notes the uneven distribution of receptors in the skin and modalities detected in the skin.
1) Pain physiology involves transduction, transmission, perception, and modulation of nociceptive signals from the periphery to the brain.
2) Pain signals are transmitted via Aδ and C nerve fibers to the spinal cord and then to the brain. Aδ fibers transmit fast, sharp pain while C fibers transmit slow, dull pain.
3) Central modulation occurs in the spinal cord and brain and can either facilitate or inhibit pain transmission and perception through mechanisms like windup, sensitization, and the release of neurotransmitters.
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.
Pain is a complex physiological process involving nociceptors, nerve fibers that transmit signals to the spinal cord and brain. The perception of pain involves multiple areas of the brain and its experience is influenced by both physiological and psychological factors. Pain signals travel through the neospinothalamic and paleospinothalamic pathways and are modulated by descending inhibitory pathways from the brain. The gate control theory explains how non-painful stimuli can reduce pain perception.
Nerve fibers are classified based on their structure, distribution, origin and function. They can be myelinated or unmyelinated. When injured, the distal portion undergoes Wallerian degeneration over 3 months as the axon and myelin sheath break down. The cell body shows chromatolysis. Regeneration is possible if the nerve ends are close together. New axonal growth occurs rapidly, entering the distal stump at 3-4mm/day. Myelination resumes over a year. Though anatomy recovers, full function returns slowly.
This document discusses pain physiology and provides definitions and classifications of pain. It describes the types of pain fibers and the pain pathway in the spinal cord. It also summarizes nociception, the modulation of pain both peripherally and centrally, and the differences between acute and chronic pain. Finally, it outlines some of the physiological effects pain can have on various body systems.
This document discusses spinal cord injuries, their classification and effects. It describes the following types of spinal cord injury: concussion, contusion, compression, laceration, hemorrhage and transection. Complete transection results in loss of all sensations and motor functions below the level of injury, causing tetraplegia or paraplegia. Incomplete injuries can cause central cord syndrome, anterior cord syndrome, posterior cord syndrome or Brown-Sequard syndrome. Brown-Sequard syndrome is caused by incomplete transection on one side and results in ipsilateral sensory and motor loss and contralateral loss of pain and temperature sensation.
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
This document provides an overview of the physiology of pain. It defines pain and discusses the dual nature of fast and slow pain. It describes the nerve pathways and brain areas involved in pain perception, as well as pain modulatory pathways and neurochemicals. The gate control theory of pain is explained, which proposes an interaction between pain and touch fibers at the spinal cord level. Factors such as referred pain and the role of capsaicin and vanilloid receptors are also summarized.
The document discusses the structure and function of chemical synapses. It begins by defining a synapse as the junction between two nerve cells. It then describes the key anatomical components of a chemical synapse, including the presynaptic knob, synaptic cleft, and postsynaptic membrane. It explains the process of neurotransmission, including the release of neurotransmitters into the synaptic cleft, their binding to receptors on the postsynaptic membrane, and the resulting postsynaptic potentials. The document also discusses inhibition at synapses, the properties of synaptic transmission, and examples of neurotransmitters.
about nerve fibers
It is the structural and the functional unit of nervous system.
The human nervous system contains approximate 1012 neurons.
A nerve fiber is a thread like extension of a nerve cell and consists of an axon and myelin sheath (if present) in the nervous system.
In peripheral nervous system it is formed by
schwann’s cell. While in case of central nervous system it is formed by oligodendroglia.
The places ,where myelin sheath is absent are called node of ranvier(2-3µm) and these are present once about 1-3 mm distance along the myelin sheath.
IT PREVENTS LEAKAGE OF IONS BY 5000 FOLDS.
IT INCREASES VELOCITY OF CONDUCTION BY 5-50 FOLDS DUE TO
SALTATORY CONDUCTION i.e. ABOUT 100 m/s IN CASE OF
MYELINATED NERVE FIBERS WHILE IN NONMYELINATED
IT IS ABOUT 0.25 m/s.
SALTATORY CONDUCTION CONSERVES ENERGY BECAUSE ONLY NODES OF RANVIER GET DEPOLARISED.
These are α type motor nerve fibers.
The neurotransmitter released at the neuron endings is acetylcholine(Ach).
It always leads to muscles excitation . Inhibition takes place centrally due to participation of interneurons.
they innervate smooth muscles , cardiac muscles and glands.
Their main work is to maintain homeostasis with the help of autonomic nervous system.
they can lead to either excitation or inhibition of effector organs
Erlanger and Grasser studied the action potential of mixed nerve trunk by means of cathode ray oscilloscope and they obtained the compounded spike. So they divided nerve fibers into 3 groups. They observed that the main cause of difference in nerve fibers is diameter
AS Diameter increases
Velocity of conduction increases.
Magnitude of electrical response increases.
Threshold of excitation decreases.
Duration of response decreases.
Refractory period decreases.
This document discusses Wallerian degeneration and nerve regeneration following injury. It begins by classifying nerve injuries according to Seddon and Sunderland's scales. It then describes the degenerative changes that occur in the distal and proximal segments of the injured axon, as well as the nerve cell body. These include fragmentation of the axon, breakdown of the myelin sheath, and chromatolysis. Eventually, axonal sprouts regenerate from the proximal segment. Peripheral nerve regeneration is aided by Schwann cells, while central nervous system regeneration faces more challenges.
A brief overview of the physiology of the neuromuscular junction.It includes a video towards the end sourced from the internet with the copyright watermarks intact.
This document provides an overview of the pathophysiology of pain. It discusses the definition of pain, pain receptors and pathways in the peripheral and central nervous systems. It describes the gate control theory of pain modulation in the spinal cord and descending pain inhibitory pathways in the brain. The document also covers physiological and psychological effects of pain, classifications of pain including nociceptive and neuropathic pain, and assessments used to evaluate pain.
The document discusses pain pathways and mechanisms. It defines pain and describes the different types of pain receptors and fibers that detect pain. The dual nature of pain as both a sensory and emotional experience is explained. Several theories of pain mechanisms are presented, including the specificity theory, pattern theory, and gate control theory. The gate control theory proposes that activity in large nerve fibers inhibits transmission of pain signals while activity in small fibers facilitates transmission. Neurotransmitters and chemical mediators involved in pain signaling are also discussed.
Nerve fibers can be classified based on their structure and distribution. There are two main types - myelinated and unmyelinated fibers. Nerve fibers also include somatic and autonomic fibers. Somatic fibers innervate skeletal muscles and the neurotransmitter is acetylcholine, leading to muscle excitation or central inhibition. Autonomic fibers innervate smooth, cardiac muscles and glands to maintain homeostasis, causing excitation or inhibition. Important properties of nerve fibers include excitability, conductivity, unfatigability, refractory periods, all-or-none response, summation, and accommodation.
Pain serves an adaptive purpose by alerting us to potential threats and motivating avoidance. It is both a sensory experience mediated by nociceptors and an emotional one. Pain becomes chronic when it persists beyond healing or when sensitization causes pain in the absence of ongoing tissue damage. Animal models are used to study pain mechanisms and test treatments given pain's complexity. Sensitization occurs peripherally by chemicals released during injury and centrally by neurotransmitters amplifying excitatory signaling in the spinal cord. Descending pathways from the brain can modulate pain transmission both up and down.
Physiology of Pain, Characteristic of pain, Basic consideration of nervous system, Pain receptor, Mechanism of pain causation, Theories of pain, Pathways of pain, Pain Receptors
- 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.
This document discusses reflex activity and the physiology of muscles and their receptors. It begins by defining a motor unit and describing the various muscle sensors, including the muscle spindle, Golgi tendon organ, and Pacinian corpuscle. It then focuses on the structure and function of the muscle spindle, its sensory and motor innervation, and its roles in proprioception and the stretch reflex. Finally, it briefly outlines muscle tone, classifications of reflexes, and preparations used to study reflexes experimentally.
This document discusses receptors and neurons that detect sensory information. It begins by defining perception and describing how sensory information is transmitted from receptors to the central nervous system. It then categorizes the different sensory modalities like touch, pain, temperature, and proprioception. The document goes on to describe the different types of sensory receptors, including their locations, the stimuli they detect, and whether they adapt rapidly or slowly. It provides examples of specific receptors like Meissner corpuscles, Pacinian corpuscles, and thermoreceptors. In closing, it notes the uneven distribution of receptors in the skin and modalities detected in the skin.
1) Pain physiology involves transduction, transmission, perception, and modulation of nociceptive signals from the periphery to the brain.
2) Pain signals are transmitted via Aδ and C nerve fibers to the spinal cord and then to the brain. Aδ fibers transmit fast, sharp pain while C fibers transmit slow, dull pain.
3) Central modulation occurs in the spinal cord and brain and can either facilitate or inhibit pain transmission and perception through mechanisms like windup, sensitization, and the release of neurotransmitters.
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.
Pain is a complex physiological process involving nociceptors, nerve fibers that transmit signals to the spinal cord and brain. The perception of pain involves multiple areas of the brain and its experience is influenced by both physiological and psychological factors. Pain signals travel through the neospinothalamic and paleospinothalamic pathways and are modulated by descending inhibitory pathways from the brain. The gate control theory explains how non-painful stimuli can reduce pain perception.
Nerve fibers are classified based on their structure, distribution, origin and function. They can be myelinated or unmyelinated. When injured, the distal portion undergoes Wallerian degeneration over 3 months as the axon and myelin sheath break down. The cell body shows chromatolysis. Regeneration is possible if the nerve ends are close together. New axonal growth occurs rapidly, entering the distal stump at 3-4mm/day. Myelination resumes over a year. Though anatomy recovers, full function returns slowly.
This document discusses pain physiology and provides definitions and classifications of pain. It describes the types of pain fibers and the pain pathway in the spinal cord. It also summarizes nociception, the modulation of pain both peripherally and centrally, and the differences between acute and chronic pain. Finally, it outlines some of the physiological effects pain can have on various body systems.
This document discusses spinal cord injuries, their classification and effects. It describes the following types of spinal cord injury: concussion, contusion, compression, laceration, hemorrhage and transection. Complete transection results in loss of all sensations and motor functions below the level of injury, causing tetraplegia or paraplegia. Incomplete injuries can cause central cord syndrome, anterior cord syndrome, posterior cord syndrome or Brown-Sequard syndrome. Brown-Sequard syndrome is caused by incomplete transection on one side and results in ipsilateral sensory and motor loss and contralateral loss of pain and temperature sensation.
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
This document provides an overview of the physiology of pain. It defines pain and discusses the dual nature of fast and slow pain. It describes the nerve pathways and brain areas involved in pain perception, as well as pain modulatory pathways and neurochemicals. The gate control theory of pain is explained, which proposes an interaction between pain and touch fibers at the spinal cord level. Factors such as referred pain and the role of capsaicin and vanilloid receptors are also summarized.
The document discusses the structure and function of chemical synapses. It begins by defining a synapse as the junction between two nerve cells. It then describes the key anatomical components of a chemical synapse, including the presynaptic knob, synaptic cleft, and postsynaptic membrane. It explains the process of neurotransmission, including the release of neurotransmitters into the synaptic cleft, their binding to receptors on the postsynaptic membrane, and the resulting postsynaptic potentials. The document also discusses inhibition at synapses, the properties of synaptic transmission, and examples of neurotransmitters.
about nerve fibers
It is the structural and the functional unit of nervous system.
The human nervous system contains approximate 1012 neurons.
A nerve fiber is a thread like extension of a nerve cell and consists of an axon and myelin sheath (if present) in the nervous system.
In peripheral nervous system it is formed by
schwann’s cell. While in case of central nervous system it is formed by oligodendroglia.
The places ,where myelin sheath is absent are called node of ranvier(2-3µm) and these are present once about 1-3 mm distance along the myelin sheath.
IT PREVENTS LEAKAGE OF IONS BY 5000 FOLDS.
IT INCREASES VELOCITY OF CONDUCTION BY 5-50 FOLDS DUE TO
SALTATORY CONDUCTION i.e. ABOUT 100 m/s IN CASE OF
MYELINATED NERVE FIBERS WHILE IN NONMYELINATED
IT IS ABOUT 0.25 m/s.
SALTATORY CONDUCTION CONSERVES ENERGY BECAUSE ONLY NODES OF RANVIER GET DEPOLARISED.
These are α type motor nerve fibers.
The neurotransmitter released at the neuron endings is acetylcholine(Ach).
It always leads to muscles excitation . Inhibition takes place centrally due to participation of interneurons.
they innervate smooth muscles , cardiac muscles and glands.
Their main work is to maintain homeostasis with the help of autonomic nervous system.
they can lead to either excitation or inhibition of effector organs
Erlanger and Grasser studied the action potential of mixed nerve trunk by means of cathode ray oscilloscope and they obtained the compounded spike. So they divided nerve fibers into 3 groups. They observed that the main cause of difference in nerve fibers is diameter
AS Diameter increases
Velocity of conduction increases.
Magnitude of electrical response increases.
Threshold of excitation decreases.
Duration of response decreases.
Refractory period decreases.
This document discusses Wallerian degeneration and nerve regeneration following injury. It begins by classifying nerve injuries according to Seddon and Sunderland's scales. It then describes the degenerative changes that occur in the distal and proximal segments of the injured axon, as well as the nerve cell body. These include fragmentation of the axon, breakdown of the myelin sheath, and chromatolysis. Eventually, axonal sprouts regenerate from the proximal segment. Peripheral nerve regeneration is aided by Schwann cells, while central nervous system regeneration faces more challenges.
A brief overview of the physiology of the neuromuscular junction.It includes a video towards the end sourced from the internet with the copyright watermarks intact.
This document provides an overview of the pathophysiology of pain. It discusses the definition of pain, pain receptors and pathways in the peripheral and central nervous systems. It describes the gate control theory of pain modulation in the spinal cord and descending pain inhibitory pathways in the brain. The document also covers physiological and psychological effects of pain, classifications of pain including nociceptive and neuropathic pain, and assessments used to evaluate pain.
The document discusses pain pathways and mechanisms. It defines pain and describes the different types of pain receptors and fibers that detect pain. The dual nature of pain as both a sensory and emotional experience is explained. Several theories of pain mechanisms are presented, including the specificity theory, pattern theory, and gate control theory. The gate control theory proposes that activity in large nerve fibers inhibits transmission of pain signals while activity in small fibers facilitates transmission. Neurotransmitters and chemical mediators involved in pain signaling are also discussed.
Nerve fibers can be classified based on their structure and distribution. There are two main types - myelinated and unmyelinated fibers. Nerve fibers also include somatic and autonomic fibers. Somatic fibers innervate skeletal muscles and the neurotransmitter is acetylcholine, leading to muscle excitation or central inhibition. Autonomic fibers innervate smooth, cardiac muscles and glands to maintain homeostasis, causing excitation or inhibition. Important properties of nerve fibers include excitability, conductivity, unfatigability, refractory periods, all-or-none response, summation, and accommodation.
Pain serves an adaptive purpose by alerting us to potential threats and motivating avoidance. It is both a sensory experience mediated by nociceptors and an emotional one. Pain becomes chronic when it persists beyond healing or when sensitization causes pain in the absence of ongoing tissue damage. Animal models are used to study pain mechanisms and test treatments given pain's complexity. Sensitization occurs peripherally by chemicals released during injury and centrally by neurotransmitters amplifying excitatory signaling in the spinal cord. Descending pathways from the brain can modulate pain transmission both up and down.
Physiology of Pain, Characteristic of pain, Basic consideration of nervous system, Pain receptor, Mechanism of pain causation, Theories of pain, Pathways of pain, Pain Receptors
- 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.
Definition n classification •Pathophysiologyof pain. •Physiological Effects of pain. •Pharmacological & non-pharmacological methods of analgesia. •Principles of pain management.METHODS OF CONTROLLING METHODS OF CONTROLLING
Non-pharmacological Preoperative counseling TENS Acupuncture
Pharmacological Opioids •Im •IV infusion •IV PCA Local anaesthetics: •Local Infiltration •Nerve Blocks •Epidural Blocks NSAIDS •IM •IV infusion •IV PCA
NON-PHARMACOLOGICAL METHODS PRE-OP COUNSELLING: Well informed patients about: •Nature of operation •Nature of post operative pain •Methods of analgesia available
Cope better with Post –op Pain
NON-PHARMACOLOGICAL METHODS TENS (Trans Cutaneous electric nerve stimulation)
Stimulates afferent myelinated (A-beta) nerve fibers at 70hz
Inhibitory circuits within sp cord activated
Nerve impulse transmission reduced
Maximum benefit in neurogenic pain
PHARMACOLOGICAL METHODS OPIODS •Activate opiodreceptors within the CNS •Reduce transmission of nerve impulses by modulation in the dorsal horn
PHARMACOLOGICAL METHODS
LOCAL ANAESTHETICS –Blocks the conduction of nerve impulses –Can be given with adrenaline because •Decreases absorption of L.A allowing larger doses •Also acts on alpha 2 receptors which potentiates analgesic effect
PHARMACOLOGICAL METHODS
NASIDS –Blocks synthesis of PG’s –Only suitable for miledto moderate pain
PRINCIPLE OF MANAGEMENT OF PAIN •Pre-emptive analgesia •Balanced or combination analgesia •Analgesia ladder
PHARMACOLOGICAL METHODS
Balanced Analgesia –NASID are used in conjunction with opioids. –Reduces amount of opioids –Reduces side affect of opioids,ASSESMENT OF PAIN •Observe the behaviour of the patient •Monitor analgesic requirement of the patient –Visual Analogue Score( VAS )
–Verbal Rating Score ( VRS ) •None •Mild •Moderate •severe
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.
The document discusses the pathways involved in analgesia and pain transmission in the central nervous system, including structures like the periaqueductal gray area, raphe magnus nucleus, and dorsal horns of the spinal cord. It also examines theories of referred pain, such as the convergence theory where nerves from somatic and visceral structures converge in the CNS. Stimulation of analgesic pathways and the release of endogenous opioids can help inhibit pain transmission.
Pain is an unpleasant sensory experience caused by actual or potential tissue damage. It serves as a warning and promotes protective reflexes. Pain is transmitted via fast-acting A-delta fibers or slow C fibers and can be localized or poorly localized. Referred pain occurs when deep pain is perceived at another site. Pain receptors are free nerve endings that transmit signals via the spinal cord and brainstem to the thalamus and cortex. The gate control theory proposes that non-painful stimuli can block pain transmission at the spinal cord. The body has endogenous analgesic systems and pathways that descend from the brain to inhibit pain.
This document provides an overview of a lecture on pain. It begins with the lecturer's name and credentials. The objectives of the lecture are then outlined, which include defining pain, differentiating between acute and chronic pain, and explaining pain management approaches. The document proceeds to discuss topics like nociceptors, the somatosensory pathway, endogenous pain mechanisms, and classifications of pain. Pathophysiological processes underlying pain are explored. Non-pharmacological pain management strategies like TENS, heat/cold therapy are also summarized.
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.
This document provides an overview of pain management in dentistry. It begins with a brief history of theories of pain and the development of pain receptors. It then discusses the neurophysiology of pain, including transduction, transmission, modulation, and perception of pain signals in the nervous system. The document outlines several theories of pain, including intensity theory, specificity theory, pattern theory, and gate control theory. It also classifies types of pain and reviews both non-pharmacological and pharmacological approaches to pain control and management in clinical settings.
Mechanism of pain | Analgesic system | Pain PhysiologyFatima Mangrio
This slideshare describes pain transduction which is the mechanism by which nociceptors depolarize to reach threshold, so that a pain signal can be transmitted to the brain. When the signal reaches the brain, the person becomes consciously aware they are in pain - this is called perception.
The document discusses the history, components, receptors, pathways, and management of pain. It provides definitions of pain and its various theories. It describes the transduction, transmission, modulation, and perception of pain. Non-pharmacological interventions like rest, modalities, and exercises are outlined. The pharmacological ladder includes non-opioid analgesics like NSAIDs that reduce inflammation. Opioids and other drug classes that help manage pain are also summarized.
The document discusses the history, components, receptors, pathways, and management of pain. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain has fast and slow components transmitted by different fiber types to the central nervous system. Management includes non-pharmacological approaches like TENS, heat, and exercise as well as pharmacological options like non-steroidal anti-inflammatories, opioids, antidepressants, and antiepileptics. The gate control theory proposes large fibers can open or close a "gate" to modulate pain transmission in the dorsal horn.
This document discusses the anatomy, physiology and management of pain. It provides details on:
- The components and pathways of the pain sensation system from nociceptors to the central nervous system.
- Theories of pain transmission including intensity, specificity and gate control theories.
- Non-pharmacological approaches to pain management such as rest, distraction, electrotherapy modalities, exercise and acupuncture.
- Pharmacological options including non-opioid and opioid analgesics.
The document discusses the history, components, receptors, pathways, and management of pain. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain has fast and slow components conducted by different fiber types to the spinal cord and brain. Nociceptors located throughout the body transduce and transmit painful stimuli. Several theories attempt to explain pain perception, including intensity, specificity, pattern, and gate control theories. Pharmacological and non-pharmacological approaches are used to manage pain, including NSAIDs, opioids, antidepressants, antiepileptics, physical therapies, and hypnosis.
1. The somatosensory system provides perception of touch, pain, temperature, and proprioception from receptors throughout the body.
2. Sensory receptors are classified as exteroceptors on the skin, proprioceptors in muscles and joints, and nociceptors for pain.
3. Sensory pathways include the spinothalamic tract for pain and temperature and the dorsal column-medial lemniscus pathway for proprioception. Lesions to these pathways result in loss of sensation on the contralateral or ipsilateral side depending on the tract affected.
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 defines pain and discusses its pathophysiology. It notes that pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Two major classes of pain are described: normal/nociceptive pain and abnormal/pathophysiologic pain. Nociception involves a complex series of physiological events between tissue damage and pain perception. Nociceptors are activated by mechanical, thermal, and chemical stimuli. The receptors that mediate pain are called nociceptors, which come in two types: Aδ myelinated nerve fibers and C unmyelinated nerve fibers. The neuroanatomy of pain processing involves afferent pathways, the central nervous system, and efferent pathways.
1) The document discusses the neuroanatomy and pathways involved in nociception and pain perception. It describes the receptors, fibers, and central processing involved in transmitting information about potentially damaging stimuli.
2) There are two main pain pathways - one transmitting fast, sharp pain via Aδ fibers and another transmitting slow, dull pain via C fibers. Both pathways involve neurons in the dorsal horn and thalamus.
3) Modulation of pain occurs via descending pathways from the brain and interactions between nociceptive and non-nociceptive fibers in the spinal cord. Dysregulation of these systems may contribute to chronic pain states.
Pain occurs when tissues are damaged and signals the body to remove the damaging stimulus. There are three main types of pain - cutaneous (skin), deep, and visceral (organ) pain - which differ in location, sensation, and pathways in the nervous system. Cutaneous pain warns of skin damage and can be fast or slow, while deep pain is dull and aching. Visceral pain is diffuse and poorly localized. Tissue damage releases chemical mediators like bradykinin that stimulate pain receptors and cause referred pain in distant areas. The intensity of pain correlates with the rate of tissue damage.
1. Brown-Séquard syndrome was first described in 1850 based on observations of machete injuries in sugar cane farmers, with key features being ipsilateral motor paralysis and mixed sensory loss below the level of the spinal cord lesion.
2. Understanding the anatomy of ascending and descending spinal tracts is important for explaining the clinical features of Brown-Séquard syndrome and other spinal cord injuries.
3. Injuries can disrupt motor or sensory tracts differently, causing varying neurological deficits depending on whether the lesion involves upper or lower motor neurons.
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The vagus nerve connects organs in the neck and below to the brainstem. It has both sensory and motor functions and helps control the heart rate, digestion, and other involuntary processes. Stimulation of the vagus nerve has been shown to reduce seizures, experimental pain, and inflammation, and may help treat conditions like epilepsy, obesity, and heart disease. Damage to the vagus nerve or its connections in the brainstem can impact swallowing, heart rate variability, and level of consciousness.
Poor water and sanitation are responsible for a huge global burden of disease, with contaminated water alone contributing to about 2.4 million preventable deaths per year, mainly in children. While progress has been made in increasing access to safe water and improved sanitation, current rates of progress will not meet the Millennium Development Goal targets. Water and sanitation remain a low priority on international development agendas despite their importance for health and achieving the MDGs. Coordinated efforts are still needed to address this critical issue.
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This document provides an overview of global health by defining key terms, outlining major players and organizations, and summarizing the history and evolution of the field from 1945 to the present day. It describes how global health has shifted from a focus on infectious disease control to addressing social determinants of health and health issues that transcend national borders. Major milestones discussed include the founding of the UN and WHO, the Alma-Ata Declaration, structural adjustment policies, the Millennium Declaration and MDGs, debt relief campaigns, and the establishment of the Global Fund. The summary highlights the ongoing tension between disease-specific and comprehensive primary healthcare approaches.
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Global health examines influences on health across borders, including issues like globalization, poverty, and human rights. It draws from multiple disciplines. Globalization refers to reducing barriers between countries, leading to increased trade, investment, and communication. This has effects like economic growth but also rising inequalities. Agreements like TRIPS have increased pharmaceutical patent protection globally, raising concerns about access to medicines, especially in developing countries. Networks of both commercial and civil society actors have been important in debates over balancing intellectual property with public health.
Migration of health care workers has both positive and negative effects on health. It reduces the availability of health services in source countries while increasing access in destination countries. This unequal distribution of health workers is driven by push factors like low pay and poor working conditions in source countries and pull factors like higher wages in destination countries. As a result, source countries experience worse health outcomes due to lack of health workers, while destination countries receive an indirect subsidy through the receipt and employment of trained medical professionals from poorer nations. Proposed policy responses aim to strengthen health systems in source countries, implement ethical recruitment practices, and foster partnerships between nations to promote more equitable health worker distribution.
Global institutions play major roles in health financing and policy. The key players discussed are the World Health Organization (WHO), World Bank, International Monetary Fund (IMF), and World Trade Organization (WTO). The WHO is the UN agency for health, working with 192 member states. The World Bank aims to reduce poverty through loans and policy advice to developing countries. The IMF promotes international monetary cooperation and provides temporary financial assistance. The WTO, formed in 1995, ensures trade flows freely through treaties and enforcement mechanisms, which some criticize can undermine public health systems.
Haemochromatosis is an autosomal recessive condition characterized by excessive iron accumulation in the body. It affects around 0.5% of Caucasians and usually presents in the 40s-50s with a triad of pigmentation, diabetes mellitus, and hepatomegaly. Diagnosis involves blood tests showing elevated serum iron, transferrin saturation over 50%, and elevated serum ferritin. Liver biopsy can confirm iron deposition and damage. Treatment aims to reduce iron stores through weekly venesection of 1 unit of blood for 6-12 months followed by maintenance venesection.
Ascites is an abnormal collection of fluid in the peritoneal cavity, commonly caused by portal hypertension due to cirrhosis. It results from sodium and water retention triggered by vasodilation and activation of the renin-angiotensin system, as well as increased hydrostatic pressure and transudation of fluid from the liver and spleen into the peritoneal cavity. Hypoalbuminemia due to decreased liver function also contributes by reducing plasma oncotic pressure. Spironolactone is used as treatment as it is an aldosterone antagonist. Management involves dietary sodium restriction, diuretics, stopping alcohol, monitoring for complications, and procedures such as paracentesis or shunts.
The liver has two lobes, separated by veins, and is divided into sections supplied by individual blood vessels. Blood flows through hepatic arteries and portal veins into sinusoids, where waste is filtered by Kupffer cells in the space of Disse before draining into hepatic veins. The liver performs many functions including synthesizing proteins, metabolizing carbohydrates and lipids, and detoxifying hormones and drugs. Liver function can be assessed through blood tests of enzymes and proteins.
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Review of orthopaedic services: Prepared for the Auditor General for Scotland...meducationdotnet
1. Orthopaedics is a large specialty that treats musculoskeletal conditions through surgery, medication, and rehabilitation. It accounts for a significant portion of NHS spending and activity in Scotland.
2. Waiting times for orthopaedic services have reduced in recent years through changes to service delivery and additional funded activity. However, further improvements to meet 18-week referral targets will be challenging to sustain.
3. There is variation in orthopaedic efficiency across Scotland that is not fully explained by resources or procedures. The report finds opportunities to use existing resources more efficiently through measures like increasing day surgery and reducing hospital length of stay.
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This document contains a series of slides related to ophthalmology. It tests the reader's knowledge on topics like visual acuity measurements, refractive errors, eye abnormalities, causes of vision loss, and eye examination techniques. The slides include images showing conditions like cataracts, glaucoma, retinal detachments, and more. Key details are provided about diagnoses, symptoms, investigations, and treatments.
2. Tpes of painy
Acute pain may be
1.Somatic
2.Visceral
3.Reffered
Chronic- long lasting
chronic diseases like arthritis.
26-Jan-16 Dr. Ashok Solanki 2
3. PAIN - NOCICEPTION
Introduction
Types of pain
Pain receptors
Pain stimulation
Fast and slow pain
Has dual feeling
Path of both types of pain is different.
Visceral pain is reffered
Lateral spinothalamic tract
Through thalamus in V.P.L.
PAIN INHIBITORY SYSTEM OF BRAIN
Sign of many underlying disease or damage.
4. a) Types of pain (somatic- fast/slow,muscular or visceral)
b) Pain pathway
c) Visceral pain & Referred Pain
d) Analgesic or pain control system of bDefinition of pain
e) Physiology of pain (properties & reaction)
f) rain & spinal cord
g) Clinical
5. a) Definition of pain
Pain sensation is unpleasant but protective sensation
aroused by noxious stimuli that damage or can damage
body tissues.
b) Physiology of pain (properties and reaction)
Purpose or importance- Protective
Stimulus- noxious (chemicals like- Ach, bradykinin,
serotonin, H,K, PGs or mechanical or thermal)
Receptors- free nerve endings (polymodal receptors)
Adaptation- non or slow adopting receptors
Nerve fibers- fast pain is carried by A-delta nerve fibers
while slow pain by ’C’ type.
6. NT-- glutamic acid (at spinal cord) for fast pain, subs P (at
spinal cord) for slow pain
Pathway- lateral spinothalamic (neo STT for fast pain
paleo STT for slow pain)
Reaction- pain is associated with muscle spasm,
withdrawal reflex (SC, fast pain), arousal (RF),
unpleasant emotions (limbic system, slow pain) and
autonomic changes- nausea, vomiting, pulse and BP
changes (hypothalamus, slow pain)
Localization & Intensity discrimination- poor but better
for fast pain
7. c) Pathways of Pain
1) From face- by trigeminal nerve (5 cranial nerve)
2) From esophagus, trachea & pharynx- 9 & 10 CN
(parasympathetic nerves)
3) From thoracic & abdominal viscera- sympathetic
nerves
4) From pelvic region- parasympathetic nerves
5) From skin of rest of the body- by free nerve endings
in lateral spinothalamic tract
8. VBC Of thalamus
thro. post. limb of IC
Primary sensory cortex
dorsal horn of spinal cord, Marginal nucleus
for fast pain & Substantia gelatinosa for slow
pain
neo STT (fast pain) & paleo STT (slow pain)
9. Origin, course & crossing
1 order neurons
Arise from receptors (free nerve endings) to dorsal horn
Of spinal cord, Marginal nucleus (MN) for fast pain &
Substantia gelatinosa (SG) for slow pain
2 order neurons
arise from MN & SG, cross to opposite side thro. Ante.
commissure & finally ascend in lateral column of SC as
neo STT (fast pain) & paleo STT (slow pain) & relay at VBC
Of thalamus & nearby st.
10. 3 order neurons
arise from VBC of thalamus (mainly fast & few slow pain
fibers) & terminate at primary sensory cortex (area 3,1,2)
Termination
All fast pain fibers & few (20%) slow pain fibers terminate
at PSC while majority of slow pain fibers, subcortically at
diffuse nuclei of thalamus, tectal nucleus & RF.
Center
Is PSC but is perceived at the level of thalamus & RF
Collaterals
To RF (aurosal), limbic system (emotion) & hypothalamus
(autonomic changes)
11. Ischemic muscle pain (SN)
- During muscle activity Lewis P factor (adenine, K &
lactic acid) pass from muscle to tissue space & clear
by blood
- But if level of Lewis P factor becomes high (ex-
during exercise) pain starts till it is cleared
Clinical-
i) intermittent claudication (leg pain on walking, when
arteries are blocked),
ii) angina pectoris (chest pain on exercise when coronary
arteries are blocked )
12. Visceral pain (SN)
Causes-
1. Over distension of hollow viscera (commonest),
2. Ischemia.
3. Obstruction
4. Spasm of hollow viscera.
Pathway-
from via type C autonomic nerves to lateral STT.
Properties-
-cause referred and radiating pain (like viscera to
peritoneum).
-more commonly associated with muscle guarding,
13.
14. -associated with unpleasant emotions and autonomic
changes (nausea, vomiting, low pulse and low BP.)
-localization & intensity discrimination is poor
-Visceras insensitive to pain-
Parenchyma of liver,
brain tissue
and alveoli of lungs are insensitive to pain.
But liver capsule, bronchi, parietal pleura & meninges
are very sensitive to pain.
15. Referred Pain (SN)
Referred Pain is the pain that is felt away from the
damaged tissue.
Dermatome rule-
visceral pain is often referred to embryonic
corresponding dermatome. The dermatome and the
visceral are innervated by the nerves arising from the
same spinal segment.
Example-
- Cardiac pain is referred to inside of the left arm.
- Pain of Appendix & ovary is referred to umbilicus,
- Diaphragm to rt. shoulder
16. 1)convergence theory of referred pain
sensory nerve carrying pain sensation from the viscera
and the sensory nerves carrying pain sensation the
dermatome converge on to same second order neuron.
17. 2) Facilitation theory of referred pain
sensory nerve carrying pain sensation from the viscera
via branches (collaterals) stimulate sensory nerve
carrying pain sensation from the dermatome. (produce
subliminal fringe effect)
18. a) Analgesic or pain control system of brain and spinal
cord Or
Mesenchephalic descending pain suppressing pathway
1. Periaqueductal grey area These fibers cause release of
encephalin & stimulates neurons in raphe nucleus
2. The raphe magnus nucleus These fibers cause release
of serotonin & stimulates neurons in spinal cord
3. Local neurons present in dorsal horns of spinal cord.
These fibers cause release of encephalin.
& encephalin causes presynaptic inhibition of pain fibers
entering into dorsal horn of spinal cord.
19.
20. Stimulants of
Analgesic system
-fibers from limbic
System,hypothalamus
-Stress, psychological
-Collaterals from pain
pathway,
-Brain opiate system
(endorphins and
encephalin)
The raphe magnus nucleus
in pons (serotonin)
Local neurons present in
dorsal horns (encephalin)
Periaqueductal grey area in
midbrain (encephalin)
presynaptic inhibition of
pain fibers in dorsal horn
21. b) Gait control theory of pain (dorsal horn of SC)
in the dorsal horn A beta, fine touch fibers cause pre-
Synaptic inhibition of pain fibers & closes the date for
pain sensation.
Role of brain in gate control
Terminals of pain fibers at dorsal horn have opiate
receptors, here descending cortical fibers can also inhibit
pain fibers & close the gate by secreting opiates
22. Clinical
Hyperalgesia- increase sensitivity to pain is known as
hyperalgesia. It may be due to:
1) primary hyperalgesia- increase sensitivity of
receptors
2) secondary hyperalgesia increase sensitivity of
pathway. (thalamic overreacton)
Hypoalgesia- is decrease sensitivity to pain while
Paralgesia is abnormal pain sensation
Acute pain (good pain) & chronic pain (bad pain)
23. Two components of pain
Fast pain is acute- 0.1 sec
Sharp pain
pricking
acute pain
burning pain
Only on superficial part
Short duration
Highly localized
Slow pain 1 sec later
Slow burning
Aching pain
Throbbing pain
Chronic pain
Prolongrd
Tissue damage or organ
Poory localized
26-Jan-16 23Dr. Ashok Solanki
24. Common causes of pain
Rise in body temp above 45
Some chemical –bradykinin
Tissue ischemia- lack of oxygen
Muscular spasm
Inflammation
5 Cardinal signs of inflammation Heat,
swelling, redness, tenderness, loss of function.
Pain has psychological aspects.
26-Jan-16 24Dr. Ashok Solanki
25. Nociceptirs- and their stimulation
Free nerve endings
Widespread
Stimuli- mechanical, electrical, chemical.
Permanent or short duration.
Slow adaptation nature
Protective
Rate of tissue damage
26-Jan-16 25Dr. Ashok Solanki
26. Pain has dual pathways
1. The sharp fast pain pathway
2. Slow – chronic pain pathway.
3. Fast by small type A delta fiber
4. Slow by type C fibers– 0.5 to 2 m/sec
5. Stimulus gives double sensation
6. Terminates on dorsal horns
7. Carried to the brain
26-Jan-16 Dr. Ashok Solanki 26
27. THE ANALGESIA SYSTEM
PREAQUEDUCTAL GRAY
RAPHE MAGNUS NUCLEUS
PAIN INHIBITORY COMPLEX IN
DORSAL HORNS
28. Referred Pain – why away from
the site of origin?
Dermatomal Rule-
embriological devlopment of
embriyo.
plasticity in the CNS coupled with
convergence of peripheral and visceral
pain fibers on the same second-order
neuron that projects to the brain.
26-Jan-16 Dr. Ashok Solanki 28
30. Dorsal Column–Medial
Lemniscal System
1. Touch sensations requiring a high degree of
localization of the stimulus
2. Touch sensations requiring transmission of
fine gradations of intensity
3. Phasic sensations, such as vibratory
sensations
4. Sensations that signal movement against the
skin
5. Position sensations from the joints
6. Pressure sensations having to do with fine
degrees
of judgment of pressure intensity
26-Jan-16 Dr. Ashok Solanki 30
32. Characteristics of Transmission in the
Anterolateral Pathway
the velocities of transmission are only one third
the degree of spatial localization of signals is
poor;
the gradations of intensities are also
far less accurate
the ability to transmit rapidly changing or
rapidly repetitive signals is poor.
is a cruder type of transmission system than the
dorsal column–medial lemniscal system.
26-Jan-16 Dr. Ashok Solanki 32
33. PAIN CONTROL (ANALGESIA)
THE ANALGESIA SYSTEM
THE BRAIN’S OPIATE SYSTEM
INHIBITION OF PAIN BY TACTILE
STIMULATION
TREATMENT OF PAIN BY ELECTRICAL
STIMULATION
REFERED PAIN
41. Structurally distinct areas, called Brodmann’s areas, of the
human
cerebral cortex.
DIVISIBLE INTO 50 AREAS.
26-Jan-16 Dr. Ashok Solanki 41
42. Referred Pain
Not at the site but superficial part of skin.
Deep somatic pain may also be referred
cardiac pain to the inner aspect of the left
arm
tip of the shoulder caused by irritation of
the central portion of the diaphragm
Important clinical sign for clinician.
Follows the Dematological rule.
26-Jan-16 Dr. Ashok Solanki 42
48. Three major pathways carry sensory
information
– Posterior column pathway
– Anterolateral pathway
– Spinocerebellar pathway
49. Role of Formation, Thalamus, Cerebral
Cortex
cortex plays an especially important role in
interpreting pain quality
strong arousal effect
a cordotomy in the thoracic region of the
spinal cord often relieves the pain
cauterize specific pain areas in the
intralaminar nuclei in the thalamus
26-Jan-16 Dr. Ashok Solanki 49
50. Transmission of Less Critical
Sensory Signals in the
Anterolateral Pathway
Carries following sensations
Pain
heat,
Cold
crude tactile
Tickle
Itch
sexual sensations
26-Jan-16 Dr. Ashok Solanki 50
52. PALEOSPINOTHALMIC TRACT
for transmitting slow- chronic pain
Slow –chronic type C fibers
Lamina 2 and 3 of dorsal horns
Joined by lamina 5.
To anterior commissure
To the opposite side of the cord
To the brain through anterolateral pathway
Substance P – the NT.
26-Jan-16 Dr. Ashok Solanki 52
57. Projection of the Paleospinothalamic
Pathway
terminates widely in the brain stem
Only one tenth to one fourth of the fibers pass all the way
to the thalamus
most terminate in one of three areas
(1) the reticular nuclei of the medulla, pons, and
mesencephalon
(2) the tectal area of the mesencephalon
(3) the periaqueductal gray region surrounding the
aqueduct of Sylvius
Then upward to the thalamus and hypoyhalamus
26-Jan-16 Dr. Ashok Solanki 57
58. Some Clinical Abnormalities
of Pain
Hyperalgesia
Herpes Zoster (Shingles)
Tic Douloureux
Brown-Séquard Syndrome
26-Jan-16 Dr. Ashok Solanki 58