The document discusses pain and the nervous system's response to harmful stimuli. It describes two waves of pain - the initial sharp pain from A-delta fibers and the longer-lasting dull pain from C-nerve fibers. It outlines the ascending pathway where pain signals travel from nociceptors to the dorsal horn and then to the brain. Chronic pain can persist after injury healing or for unknown reasons, and can be caused by various physical and neurological conditions.
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 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.
The document discusses pain psychology and pain management over several pages. It begins by defining pain and describing the physiology of pain, including pain receptors and the gate control theory of pain. It then discusses psychological factors that can influence pain like learning, personality, and cognition. The document covers various methods for managing pain, including medications, surgery, physical therapies, hypnosis, biofeedback, relaxation techniques, and cognitive behavioral approaches.
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 pathophysiology and methods of pain control. It begins by classifying pain based on duration, intensity, etiology, and other factors. It then describes the anatomy and physiology of pain pathways, including transduction, transmission through the peripheral and central nervous system, and modulation. This involves nociceptors, dorsal root ganglia, spinal cord dorsal horn, and brain structures. Finally, it discusses various pharmacological and non-pharmacological methods for pain control, such as paracetamol, NSAIDs, opioids, antidepressants, and more.
Dr. Shekhar Anand presented on methods of chronic pain management to the Department of Anesthesiology. He discussed that chronic pain is defined as pain lasting longer than 3-6 months and can be nociceptive, neuropathic, or mixed in nature. Chronic pain is best managed using a multidisciplinary approach including pharmacological interventions like opioids, antidepressants, anticonvulsants, as well as non-pharmacological therapies like cognitive behavioral therapy, physical therapy, and interventional procedures. The goals of chronic pain management are to improve function and quality of life, rather than to cure the underlying cause of pain.
Trauma or injury causes the release of chemicals that stimulate nerve fibers, leading to pain signals being sent to the brain. The integration of these pain signals with cognitive, emotional, and environmental factors results in the perception of pain. When this balance is disturbed, chronic pain can develop. Chronic pain is defined as pain lasting beyond normal tissue healing time, typically three months. A multidisciplinary approach is often needed to treat chronic pain through non-pharmacological and pharmacological methods.
This document discusses different types of pain. It describes fast pain, which occurs within 0.1 seconds and is transmitted quickly, and slow pain, which takes over 1 second to start and increases slowly over minutes, being transmitted more slowly. Fast pain includes sharp and electric pain in superficial tissues, while slow pain includes aching and chronic pain that can occur deep in tissues. Pain signals travel along dual pathways in the spinal cord and brainstem. The document also discusses visceral pain referral and its causes from internal organ damage or stretching.
Pain Management (General concepts and primary discussions)Saeid Safari
This document provides an overview of pain medicine. It defines pain and discusses its epidemiology, economics, and physiological effects. It describes acute and chronic pain, including their presentations and pathophysiology. Neuropathic and nociceptive pain are major categories discussed. Pain pathways and the gate control theory of pain are also summarized. Psychiatric comorbidities with chronic pain are noted.
This document discusses chronic pain management. It defines chronic pain as pain that lasts months or years in any part of the body and can lead to depression, anxiety, and sleep issues. Chronic pain differs from acute pain in that it continues long after an injury heals. The document describes three types of chronic pain - neuropathic, somatic, and visceral - and their characteristics. It discusses evaluating and measuring pain, as well as pharmacological, physical, psychological, and invasive treatment methods for managing chronic pain. The goal of chronic pain treatment is to improve daily functioning and quality of life by decreasing pain and suffering through a multidisciplinary approach.
Post-operative pain management involves a multimodal approach to minimize pain and reduce opioid use and side effects. This includes pre-operative planning, various regional anesthesia techniques during surgery, and post-operative pain control using opioids, non-opioid analgesics, and patient-controlled analgesia. Proper pain management improves patient outcomes and satisfaction while reducing complications after surgery.
Pain as an unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such
The document discusses several theories of pain including:
1) Specificity theory which proposed specialized pain receptors
2) Gate control theory which proposes that pain is modulated by a "gate" in the spinal cord that can be opened or closed by non-painful stimuli
3) Neuromatrix theory which suggests that a person's unique matrix of neurons is shaped by their physical, psychological, and cognitive traits and experiences.
It also discusses pain control mechanisms like endogenous opiates and placebos, and provides examples of how integrating pain theories can guide multimodal pain management strategies.
1. The document discusses pain, defining it as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
2. Pain is always subjective and can be somatic, visceral, or neuropathic in nature. It can be acute or chronic, with chronic pain lasting over 3 months and having a large psycho-social component.
3. The gate control theory proposes that psychological factors can affect the experience of pain by opening and closing a "gate" in the spinal cord that modulates pain transmission.
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.
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 definitions, classifications, physiology, assessment, and management. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is classified based on location, duration (acute vs chronic), and intensity (mild, moderate, severe). The physiology of pain involves transduction, transmission, modulation, and perception of pain signals in the nervous system. Nurses assess pain using scales and treat it using pharmacological and non-pharmacological methods based on the type and severity of the pain.
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.
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.
Pain pathway gate control theory
Pain management
An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to CNS where it is interpreted as such.
1. Exteroceptors: arising from receptors from skin & mucosa. sensed at conscious level
E.g. Merkel corpuscles : Tactile receptors.
Free Nerve ending :Perceive superficial pain.
2. Proprioceptors : From musculoskeletal structures.
The presence , positions & movement of body. below conscious levels.
E.g. 1) Muscle spindles : Skeletal muscle fibers. Mechanoreceptors.
2) Free nerve ending : Perceive deep somatic pain & other sensations.
3. Interoceptors : From viscera of body below conscious level.
E.g. Pacinian corpuscles : perception of touch-pressure.
Free nerve ending : Perceive visceral pain & other sensations.
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.
The document discusses pain and its classification, pathways, and treatment. It defines pain and describes the gate control theory of pain modulation. Pain is classified as nociceptive, neuropathic, or idiopathic. Treatment includes non-opioids like NSAIDs, opioids like morphine, and adjuvants. Morphine is a potent analgesic that acts primarily on mu opioid receptors in the CNS and PNS to reduce pain perception. Its mechanisms, effects, kinetics, uses, and adverse effects are outlined.
This document discusses the pathophysiology of pain. It begins with an introduction that defines pain and discusses pain perception. It then covers the pathophysiology of pain perception including transduction, transmission, modulation, and the physiological effects of pain. The document classifies pain into nociceptive, neuropathic, and referred pain, and by duration as acute or chronic. It concludes with a discussion of pain assessment methods.
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.
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
This document discusses pain pathways in the human body. It begins with definitions of pain from various sources and an overview of the functional anatomy and neurophysiology of pain. It then covers topics like neurochemistry of nociception, theories of pain, pain modulation, types of pain, and factors affecting the pain response. Diagrams are provided to illustrate concepts like nociceptor types and locations, nerve fiber types and velocities, synaptic transmission of pain signals in the dorsal horn and pathways to the brain. The gate control theory of pain and mechanisms of central modulation of pain are also summarized.
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.
Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is classified in several ways including by type (nociceptive, neuropathic, psychogenic), duration (acute, chronic), and location. Theories of pain transmission include the specificity, pattern, and gate control theories. Pain signals travel along A-delta and C fibers to the spinal cord and then ascend to the brain via the spinothalamic tract. Descending pathways from the brainstem modulate pain transmission through the release of neurotransmitters like serotonin and norepinephrine.
This document summarizes the pain pathway. It begins with definitions of pain and discusses pain receptors called nociceptors. It describes the different types of stimuli that can activate nociceptors as well as the different classifications of pain. The document then outlines the nerve pathways that carry pain signals from the periphery to the brain, including nociceptive fibers, dorsal horn synapses, and ascending tracts. It also discusses descending pain modulation and theories of pain transmission like the gate control theory.
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.
This document discusses pain anatomy and physiology. It defines pain as an unpleasant sensory and emotional experience associated with tissue damage. Nociception is the process by which nociceptors detect and transmit signals of potential tissue damage to the brain. There are different types of nociceptors and pain fibers that detect fast, sharp pain or slow, dull pain. The ascending pain pathway involves three neurons that transmit nociceptive signals from receptors to the spinal cord and thalamus. The gate control theory proposes that non-painful input can close the "gates" and inhibit pain transmission.
This document provides an overview of pain, including definitions, mechanisms, and assessment. It discusses the levels of pain processing from transduction to perception. The functional neuroanatomy and pathways of pain are described, including nociceptors, nerve fibers, spinal cord tracts, and brain regions involved. Modulation of pain within the central nervous system is explained through theories like the gate control theory. Methods of pain assessment and various types of pain are also summarized.
This document discusses several theories of pain perception, including intensity theory proposed in 1874, specificity theory proposed in 1895, and pattern theory proposed in 1894. It also describes gate control theory proposed in 1965, which postulates that non-painful stimuli can close the "gate" and inhibit pain signals in the spinal cord. Finally, it discusses the hydrodynamic theory from 1966, which is the most widely accepted explanation for tooth sensitivity involving the movement of fluid in dentinal tubules activating nerve fibers.
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 provides a tutorial on spike sorting using the wave_clus graphical user interface. It outlines the spike sorting method which involves spike detection using amplitude thresholding, feature extraction using wavelets, and sorting using superparamagnetic clustering. The tutorial walks through loading simulated data into wave_clus, exploring clustering and parameter changes, and provides guidance on sorting real neural data recorded from epilepsy patients. The goal is to demonstrate the wave_clus software and spike sorting workflow to automatically detect and separate spikes from different neurons.
Emotion involves interactions between the peripheral nervous system, brainstem, hypothalamus, limbic system, and cortex. The amygdala and hypothalamus play key roles in processing fear and anxiety through their connections to the autonomic nervous system. Aggression can involve the hypothalamus, midbrain, amygdala, and serotonin systems. Current research shows that emotions emerge from activity across distributed neural circuits rather than isolated centers.
Emotion involves interactions between the peripheral nervous system, brainstem, hypothalamus, limbic system, and cortex. The amygdala and hypothalamus play key roles in processing fear and anxiety through their connections to the autonomic nervous system. Aggression can involve the hypothalamus, midbrain, amygdala, and serotonin systems. Current research shows that emotions emerge from activity across distributed neural circuits rather than isolated centers.
The document discusses language and the brain. It covers what language is, how it is processed in the brain through sensory and motor systems, and the localization of language functions in different brain areas like Broca's area and Wernicke's area. Studies of patients with aphasia from brain damage helped uncover that distinct types of aphasia suggest language is processed in multiple stages across different brain regions.
This document discusses the chemical senses of taste and smell in humans. It describes the different types of chemoreceptors in the body and focuses on those related to taste and smell. It explains the basic tastes detected by taste buds on the tongue and how taste is transduced. It also describes the organs and cells involved in smell, including olfactory receptors in the nose, and how odors are transduced. Neural pathways that transmit signals from taste buds and olfactory receptors to the brain are outlined.
The vestibular system in the inner ear detects motion and orientation of the head to maintain balance. It contains semicircular canals that detect rotational head movement and otolith organs that detect linear acceleration. Signals from the vestibular system are integrated with other sensory inputs in the brainstem and cerebellum to coordinate eye movements and posture. Damage to the vestibular system can cause vertigo and loss of balance.
The auditory system allows humans to perceive sound. Sound waves enter the outer ear and vibrate the eardrum, transmitting vibrations through three small bones to fluid in the inner ear. Hair cells in the cochlea convert vibrations into nerve signals about sound frequencies and intensities. The brain processes these signals to perceive qualities like pitch and loudness. Damage to hair cells or nerves can cause hearing loss while cortical damage may impact speech understanding.
This document discusses the chemical senses of taste and smell in humans. It describes the different types of chemoreceptors in the body and focuses on those related to taste and smell. It provides details on the organs, cells, neural pathways and mechanisms of taste and smell transduction. It also compares taste and smell systems between humans and other animals.
The document discusses different techniques for improving memory, including recognizing images, remembering faces, associating new information with existing memories, and creating mental images and stories to connect items. It describes experiments that showed creating elaborate encodings by connecting new information to existing knowledge helps move information from short-term to long-term memory better than repetition alone.
The document discusses the history and key concepts of cognitive science, including how different sensory systems process information and how perception is constructed. It covers early pioneers like Ebbinghaus who studied memory and Pavlov who demonstrated classical conditioning. Pavlov's work showed how a neutral stimulus could elicit a response through repeated pairing with an unconditional stimulus. Later, theorists like Watson focused on observable behaviorism while cognitive psychology emphasized that perception depends on internal representation and mental structures.
This document summarizes molecular mechanisms of learning and memory, including procedural and declarative memory systems, and models like Aplysia and cerebellum that are used to study these mechanisms at the neuronal and molecular level. It discusses various forms of learning like habituation, sensitization, and classical conditioning; and memory mechanisms like long-term potentiation and long-term depression that involve modification of synaptic strength through molecular cascades and changes in gene expression.
1. Memory involves multiple brain structures working together, including the hippocampus, medial temporal lobe, striatum, thalamus, and neocortex.
2. Visual information is first processed in the visual cortex, then held in short-term memory in the frontal lobes.
3. The hippocampus stores new information from short-term memory for weeks or months before transferring it to the cerebral cortex for long-term storage.
4. Recalling long-term memories routes information from the cerebral cortex back to the frontal lobes for temporary storage in working memory.
This document summarizes the spinal control of movement. It discusses how motor neurons innervate skeletal muscles and are wired into reflex loops in the spinal cord. The spinal cord also contains central pattern generators that provide rhythmic patterns for activities like walking. Skeletal muscle contraction is enabled by the sliding filament model where actin and myosin interact through a cross-bridge cycle powered by ATP hydrolysis. Motor neurons and calcium signaling control muscle contraction and relaxation.
The brain controls movement through a hierarchy with three levels - strategy, tactics, and execution. The highest level of strategy is in the neocortex and basal ganglia. Tactics are handled by the motor cortex and cerebellum. Execution occurs via signals from the brainstem and spinal cord to muscles. Sensory feedback is essential at each level. Voluntary movement involves cortical areas planning strategies that activate the basal ganglia and cerebellum to initiate and coordinate movement signals sent to the spinal cord.
The document discusses several animal senses that differ from human senses, including echolocation, electroreception, chemoreception, vision beyond the visible light spectrum, infrared vision, magnetoreception, and head tracking in chickens. Echolocating animals like bats use echo location to navigate and hunt by emitting calls and interpreting the returning echoes. Electroreception allows some aquatic animals to detect electric fields for navigation and hunting prey. Various animals have enhanced chemoreception, vision, infrared detection and magnetoreception abilities compared to humans.
Yeah, i'm too lazy to open up adobe...
enjoy!
(I hear NSHS has a record number of students attending this year!)
[which means that ass kicking is mandatory]
The document provides an overview of the anatomy and physiology of the human visual system. It describes the main components of the eye, including the retina, cornea, lens, iris, and optic nerve. It explains how light enters the eye and is focused on the retina, and how photoreceptors in the retina convert light into neural signals sent to the brain via the optic nerve. It then discusses visual processing in the lateral geniculate nucleus and primary visual cortex, including retinotopic mapping and different pathways for color, motion, and shape processing.
1) The brain continues developing through adolescence and early adulthood, with significant changes occurring in brain structure and function during this period.
2) Puberty triggers a cascade of hormonal changes that influence brain development in both direct and indirect ways. Areas of the brain involved in self-regulation and risk-taking, such as the prefrontal cortex, are among the last to fully mature.
3) Adolescents tend to engage in more risk-taking behaviors than children or adults, which may be explained by an imbalance between the earlier maturation of the brain's reward system versus the later maturation of self-control regions.
The human nervous system begins developing at 3 weeks when the neural plate starts to thicken and fold in to form the neural tube. Critical periods of development occur when neurons determine their specific functions. By birth, the brain contains around 100 billion neurons that develop through processes of proliferation, migration, differentiation, and apoptosis to form neural circuits and connections influenced by genetic and environmental factors.
The document discusses infant brain development from birth through early childhood. It notes that neurons develop rapidly before birth and connections between neurons multiply greatly in the first few months of life. Early experiences physically determine how the brain is wired, as connections are strengthened through repetition and pruned if not used. The brain is most plastic and able to learn during the first three years. Deprivation can negatively impact brain development, while sensory stimulation, secure attachments, and adequate sleep support healthy development.
Hemodialysis: Chapter 8, Complications During Hemodialysis, Part 2 - Dr.GawadNephroTube - Dr.Gawad
- Video recording of this lecture in English language: https://youtu.be/FHV_jNJUt3Y
- Video recording of this lecture in Arabic language: https://youtu.be/D5kYfTMFA8E
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Why Does Seminal Vesiculitis Causes Jelly-like Sperm.pptxAmandaChou9
Seminal vesiculitis can cause jelly-like sperm. Fortunately, herbal medicine Diuretic and Anti-inflammatory Pill can eliminate symptoms and cure the disease.
Chair and Presenter, Stephen V. Liu, MD, Benjamin Levy, MD, Jessica J. Lin, MD, and Prof. Solange Peters, MD, PhD, prepared useful Practice Aids pertaining to NSCLC for this CME/MOC/NCPD/AAPA/IPCE activity titled “Decoding Biomarker Testing and Targeted Therapy in NSCLC: The Complete Guide for 2024.” For the full presentation, downloadable Practice Aids, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at https://bit.ly/4bBb8fi. CME/MOC/NCPD/AAPA/IPCE credit will be available until July 1, 2025.
Ontotext’s Clinical Trials Eligibility Design Assistant helps with one of the most challenging tasks in study design: selecting the proper patient population.
Causes Of Tooth Loss
PERIODONTAL PROBLEMS ( PERIODONTITIS, GINIGIVITIS)
Systemic Causes Of Tooth Loss
1. Diabetes Mellitus
2. Female Sexual Hormones Condition
3. Hyperpituitarism
4. Hyperthyroidism
5. Primary Hyperparathyroidism
6. Osteoporosis
7. Hypophosphatasia
8. Hypophosphatemia
Causes Of Tooth Loss
CARIES/ TOOTH DECAY
Causes Of Tooth Loss
CAUSES OF TOOTH LOSS
Consequence of tooth loss
Anatomic
Loss of ridge volume both height and width
Bone loss :
mandible > maxilla
Posteriorly > anteriorly
Anatomic consequences
Broader mandibular arch with constricting maxilary arch
Attached gingiva is replaced with less keratinised oral mucosa which is more readily traumatized.
Anatomic consequences
Tipping of the adjacent teeth
Supraeruption of the teeth
Traumatic occlusion
Premature occlusal contact
Anatomic Consequences
Anatomic Consequences
Physiologic consequences
Physiologic Consequences
Decreased lip support
Decreased lower facial height
Physiologic Consequences
Physiologic consequences
Education of Patient
Diagnosis, Treatment Planning, Design, Treatment, Sequencing, and Mouth Preparation
Support for Distal Extension Denture Bases
Establishment and Verification of Occlusal Relations and Tooth Arrangements
Initial Placement Procedures
Periodic Recall
Education of Patient
Informing a patient about a health matter to
secure informed consent.
Patient education should begin at the initial
contact with the patient and should continue throughout treatment.
The dentist and the patient share responsibility for the ultimate success of a removable partial denture.
This educational procedure is especially important when the treatment plan and prognosis are discussed with the patient.
Diagnosis, Treatment Planning, Design, Treatment, Sequencing, and Mouth Preparation
Begin with thorough medical and dental histories.
The complete oral examination must include both clinical and radiographic interpretation of:
caries
the condition of existing restorations
periodontal conditions
responses of teeth (especially abutment teeth) and residual ridges to previous stress
The vitality of remaining teeth
Continued…..
Occlusal plan evaluation
Arch form
Evaluation of Occlusal relationship through mounting the diagnostic cast
The dental cast surveyor is an absolute necessity in which patients are being treated with removable partial dentures.
Mouth preparations, in the appropriate sequence, should be oriented toward the goal of
providing adequate support, stability,
retention, and
a harmonious occlusion for the partial denture.
Support for Distal Extension Denture Bases
A base made to fit the anatomic ridge form does not provide adequate support under occlusal loading.
The base may be made to fit the form of the ridge when under function.
Support for Distal Extension Denture Bases
This provides support
Descoperă Bucuria Vieții Sănătoase cu Jurnalul Fericirii Life Care - Iulie 2024!
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Sfaturi practice pentru o alimentație sănătoasă:
Rețete delicioase și ușor de preparat: Bucură-te de preparate gustoase și nutritive, perfecte pentru zilele călduroase de vară.
Recomandări pentru o alimentație echilibrată: Asigură-ți aportul necesar de nutrienți esențiali pentru un organism sănătos și plin de vitalitate.
Sfaturi pentru alegeri alimentare inteligente: Învață cum să faci cumpărături sănătoase și să eviți tentațiile nesănătoase.
Trucuri pentru un stil de viață activ:
Rutine de exerciții fizice adaptate nevoilor tale: Găsește antrenamente potrivite pentru a te menține în formă și energic pe tot parcursul verii.
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Sfaturi pentru o stare de bine mentală:
Tehnici de relaxare și gestionare a stresului: Învață cum să te relaxezi și să faci față provocărilor zilnice cu mai multă ușurință.
Sfaturi pentru cultivarea optimismului și a gândirii pozitive: Descoperă cum să abordezi viața cu o perspectivă optimistă și să atragi mai multă bucurie în ea.
Recomandări pentru a te conecta cu natura: Bucură-te de beneficiile naturii asupra stării tale mentale și emoționale.
Bonus:
Oferte exclusive la produsele Life Care: Beneficiază de reduceri și promoții speciale la o gamă largă de produse pentru o viață sănătoasă.
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Jurnalul Fericirii Life Care - Iulie 2024 este mai mult decât o simplă revistă. Este un ghid complet și personalizat pentru a te ajuta să obții o viață mai sănătoasă, mai fericită și mai plină de satisfacții.
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Finally, the lecture includes a case study to apply theoretical knowledge to a practical scenario, helping students understand the real-world implications of coronary circulation and ischemic heart disease. The role of biochemical factors in cardiac pain and the interpretation of ECG changes in myocardial infarction are also covered.
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2. The nervous system’s response to noxious (harmful) stimuli, also known as “nociception” Examples of external stimuli: pricking, cutting, crushing, burning, freezing Examples of internal stimuli: swelling, inflammation, distention (Note: These are noxious stimuli, but other stimuli must cause these stimuli—swelling, for instance, does not usually happen on its own) Several factors contribute to reception of pain Mechanical stimulation from sharp object Potassium released from the insides of the damaged cells Prostaglandins, histamines, and bradykinin from immune cells that invade area of inflammation Substance P from nearby nerve fibers So, What is Pain, Anyway?
3. There are Two “Waves” of Pain Nociceptors Free nerve endings (dendrites) in the skin that pick up the information from the painful stimuli Only responds to extreme pressure or temperature Found almost everywhere: from skin to teeth pulp to joint membranes to muscles Nociceptors are the dendrites of nerve fibers There are two types of axons of these nerve fibers A-delta fibers C-nerve fibers (two types) Both travel relatively slowly compared to other peripheral axons
4. A-DELTA NERVE FIBERS First wave of pain (initial pain—sharp and highly localized) Thick(er) and myelinated (moderately fast transmission) Limited to responses from very strong pressure and extreme temperatures (tend to be from immediate stimuli) C-NERVE FIBERS Also known as “Polymodal nociceptors” Second wave of pain (longer-lasting, duller, widespread pain) Very thin and unmyelinated (very slow transmission) Not limited to immediate stimuli—also respond to chemicals released by cells already damaged by burns, wounds, and infections ( this accounts for their long-lasting effect)
5. Just a little touch/pain humor…. … .and something else to ponder.
6. Notice that the nociceptors labeled here are located in the EPIDERMIS and that they are FREE NERVE ENDINGS, or afferent nerve dendrites that are not encapsulated (as touch, heat, and pressure nerve endings are) Cutaneous (“In the Skin”) Receptors
7. Pain’s Ascending Pathway to the Brain A-delta fibers and C-nerve fibers form synapses with dorsal horn of spinal cord Cell bodies in dorsal root ganglia Synapse between primary pain-sensing neurons and secondary pain-transmission neurons occurs in dorsal horn of spinal cord Secondary neurons send signals upward through spinothalamic tract Contralateral side of spinal cord Face sends info through “mini-spinal cord” called trigeminal nerve into the medulla
8. Proposed by Ronald Melzack and Patrick Wall Grew out of observations of WWII veterans and their injuries Concept: pain messages are intercepted by specialized nerve cells in the spinal cord before they reach brain For severe pain that could lead to damage Nerve “gate” is wide open Message travels almost instantaneously For mild, weak pain Nerve gate sometimes closed Filter, block pain messages Gate Control Theory
9. Nerve fibers that transmit touch influences gatekeeper cells Touch stimulate gatekeeper cells to close “gate” Decrease pain transmission Rubbing sore area = relief Gate Control Theory Cont’d
10. Pain and normal somatosensory neurons both synapse on projection cells (which go up into brain) and inhibitory interneurons in spinal cord Normal somatosensory signals turns on both projection and inhibitory neurons= cancel each other out Only pain turns on projection and inactivates the inhibitory- leading to pain Gate Control Theory: In-Depth
12. When humans’ brains are mapped for response to lasers, this area activates. While controversial, one area, the Vmpo, causes pain or temperature-related sensations when stimulated. It gets messages from lamina I through the thalamus. Lesions in the parieto-insular cortex reduces pain. The Parieto-Insular Cortex
13. Medial Frontal Cortex This is part of an area involved in controlling motivational behavior It activates in response to perceiving the unpleasantness of pain
14. The parieto-insular cortex is responsible for the physical sensation processing The anterior cingulate is responsible for the emotional response to pain This theory suggests that pain in primates is “phylogenetically novel” because involved areas are large in primates, but especially large in humans It could explain the effects of pain and the autonomic system on feelings Simpler animals experience pain in the brainstem, but do not experience it cortically One Possible Theory
15. The Descending Pathway Descending system suppresses the transmission of pain signals from the dorsal horn of spinal cord to higher brain centers Originate in the somatosensory cortex and hypothalamus Thalamic neurons suppress ascending nerve signals at synapses in midbrain Periaqueductal Gray Also stimulate release of natural chemicals in body….
16. The Neurotransmitters of PAIN Nerves transmitting pain signals, as well as those involved in pain regulation, use excitatory and inhibitory neurotransmitters Excitatory Neurotransmitters of Pain Signaling Glutamate— -NMDA , AMPA, and metabotropic receptors are involved in excitatory synaptic transmission of pain. -With NMDA (C-fibers), Mg++ clogs receptor -Nearby peptide receptors stimulated channel opens -Depolarizes the neuron Tachykinins— -G-protein coupled receptors -Neurokinin A binds to NK-2 receptors, and Neurokinin B binds to NK-3 receptors
17. Substance P (The “P is for Pain” Molecule), a Tachykinin -Found in C-fibers -First described by von Euler & Gaddum in 1931 during research of equine brain and intestines -Sequenced in 1971 -Binds to NK-1 receptors , but is synthesized by nociceptors -Vasodilation (swelling of capillaries) and release of histamine by mast cells (see below) Neurotensin -Detected during isolation of Substance P from bovine samples -Causes vasodilation in already-open wounds Histamine -In mast cells of the immune system; subtance P and foreign substances like bee venom cause release onto nociceptors, triggering depolarization -Also “punctures” blood capillaries, causing swelling and redness at location of injury
18. ATP -Released by damaged cells and binds to ATP-gated channels on nociceptors (then the cell is depolarized...) -Neurotransmitter associated with prostaglandin (a hormone) H+—from build up of lactic acid, activate H+-gated channels Potassium Ions -Released by damaged cells; indirect depolarization of nociceptors Proteases -Break down kininogen from outside cell into bradykinin, which binds to receptors opening ion-gated channels Calcitonin and other neuropeptides (there are MANY that are related) NOTE: THESE ONLY APPLY TO CERTAIN A-DELTA AND C-FIBERS -There are certain c-fibers known as IB 4 -positive fibers, which so far only seem to bind to plant isolectin
19. Inhibitory Neurotransmitters of Pain Signaling Most important: GABA -Ligand-gated and G-protein coupled receptors -Most important for interneurons (gate-control theory) Glycine Neurotransmitters Mediating Pain Regulation -Serotonin and Norepinephrine are involved in transmission between neurons of the descending pathway -Often working in tandem with Substance P
20. A Remarkable Discovery with Fos Shows up in the spinal cord after even brief noxious stimulation, particularly of C-nerve fibers, but disappears after 2-7 days; expression of C-Fos gene in damaged nerves that do not typically express Fos An Inducible Transcription Factor, which changes the internal environment of the cell on a long-term basis Therefore, provides a link between persistent stimulation and consequences for the future by gene expression! Although the transcription of C-Fos is understood generally, its precise mechanisms involving neurons, especially concerning cell Replication, are not quite understood
21. How the Pain We Feel is Different Different types of nerves and neurotransmitters Nociceptors are simultaneously activated with other cutaneous receptors, like mechanoreceptors, giving us: -Pressure-pain -Hot-pain -Cold-pain -Etc. As for spicy foods….
22. Spicy Foods are Moderated by Capsaicin First isolated as a vanilloid in red peppers (then chilies, jalapeños….) Simultaneous activation of nociceptors by capsaicin and taste receptors by other ingredients provides for different “types” of spicy Selective activation of C-fibers (and sometimes A-delta fibers) Depolarization of unique ion-gated channel with “vanilloid” receptor -VR1, vanilloid receptor subtype 1 has a very specific antagonist, capsazepine “ Excitotoxin”-death of neurons of the dorsal root ganglion with prolonged exposure BUT just the right amount of repeated application results in depletion of substance P
23. Pain that lasts 6 months or longer Persists long after trauma has healed or in the absence of trauma Common causes of chronic pain Physical problems stemming from chronic illness or internal injuries Arthritis: inflammation of the joints Damage to peripheral or spinal nerves Neuropathic pain Can result from accidents, infections, surgery Unknown cause (possibly psychological?) Chronic Pain
24. Autoimmune Diseases MS, lupus Cancer Compression/ Trauma Crush nerves Diabetes Most common Drug side effects Nutritional Deficiencies Infectious Disease Lyme disease, herpes, HIV Toxic Substances Mercury, lead, arsenic More Causes of Pain and Nerve Damage
25. “ Off” Perception of Pain Allodynia—“painful” response to a typically non-painful stimulus Hyperalgesia—increased “painful” response to a painful stimulus Pain Enhancement during illness Stops person from wasting energy Immune system interaction? Pain Enhancement after Injury Damage to/recent activation of nocioceptors respond to weaker stimuli (use of local anesthetics) Stops person from touching wounds/getting infections Sensitization
26. Nervous system amplifies and distorts pain Resulting pain out of proportion to original injury or disease Causes Inflammation: nociceptors fire w/ greater intensity, longer time, lower threshold Abnormal chemical reactions in spinal cord that increase transmission of pain messages Lower threshold of pain receptors Examples of Sensitizers: bradykinin, prostaglandins, and substance P Linked to sensing, feeling, and thinking regions of brain Leading to emotional, psychological suffering
27.
28. But Don’t Forget the Most Curious Substance of All..... ~Endorphins, or End ogenous M orphin e-like Substances In the late 60s, researchers identified the so-called opioid receptors: mu, kappa, and delta Increasing identification of opioid antagonists (ex. Naloxone) We must have a natural substance in our brain such that we would from an evolutionary perspective require, or at least benefit from, the presence of opioid receptors In and around 1975, discovery of the Met-enkephalins (Methionine), Leu-enkephalins (Leucine), dynphins, and Beta-endorphin, which bind to opioid receptors -Proenkephalins are produced by the cell body then split into active peptides -Enkephalins then hyperpolarize the neuron by inhibiting excitatory neurotransmitters
30. Ascending Regulation Simultaneous activity in A-beta fibers (low-threshold mechanoreceptors) ex. Massaging bruises Descending Regulation Electrode Therapy Perhaps most important: electrical stimulation of the PAG Input from the thalamus and other structures Medulla, especially raphe nuclei, using serotonin back to dorsal horn of spinal cord
31. Drug-Mediated Management Partial and full opioid agonists ex. Morphine, heroine, fentanyl, oxycodone, demerol Nerve terminals of primary pain neurons in dorsal horn contain opioid receptors, activation of which inhibits transmitter release Injection of opioids into midbrain can cause profound pain relief (connected to primary pain neurons) CCK Antagonists Mu receptor activation releases CCK, which goes on to inhibit opioid effects (through activation of other substances, such as substance P) Corticosteroids (anti-inflammatory medications) Capsaicin (sounds counterintuitive, I know….) Anesthetics (nitrous oxide, PCP, cocaine) Cannabis
32. NSAIDs Inhibit prostaglandin Tend to inhibit all prostaglandin—analgesia and anti-inflammation, but no muscle regeneration Anti-Histamines Reduce swelling and irritation at injury site Antidepressants Stress-Induced Analgesia Endorphins Suppress glutamate and hyperpolarize neurons In response to stress and physical exertion Belief-Induced Analgesia “ Placebo Effect” Other Therapies Surgery (an extreme) Psychedelics and caffeine for headache relief Alternative Therapies: hot/cold compresses, chiropracty, massage, hypnosis, herbal medicines, acupuncture
33. Pain Tolerance Pain tolerance is generally higher in men than in women, and decreases with age In men pain tolerance increases significantly in repeat testing Researchers expect that gender role expectations effect how men perform on the test A woman’s ability to handle pain may also relate to where she is in her hormone cycles In animal studies it was found that females have fewer opioid receptors than males, which may account for gender differences.
34. More connections to regions of the brain associated with external functions More connections to regions of the brain associated with internal functions
37. Phantom limb pain—pain without stimuli or receptors Ramachandran Destruction of nerves and pain modulation Mirror therapies
38. SCN9A, CIPA and Evolution SCN9A instructs the protein sodium channel that allows neurons to pass on messages In a study of children where this was faulty, scientists found that they felt no pain They frequently bit their lips and two of them had bitten at least a third of their tongue off. In fact, one girl thought it was funny to bite her fingers and see the blood.
39. In a study of people who had too much of SCN9A, the people experienced chronic burning in their extremities
40. CIPA is a nerve disorder in which the nerves for sensing temperature and pain don’t form Mutations of the NTRK1 gene—NGF binding to TrkA receptor on nociceptive and sympathetic nerves not encoded Some estimate that CIPA affects approximately one in 125,000,000 Issues: Common infections -> amputation Accidentally biting tongue through or clean off when eating Dying of overheating
41. Bibliography Andreae-Jones, Sarah, MB BS. “Capsaicin, Corticosteroids, and CCK Antagonists.” A.S.A.M. Society . July 2000. < http://www.arachnoiditis.info/content/capsaicin_corticosteroids_cck_antagonists/capsaicin_cortico steroids_cck_antagonists.html >. 2 Feb. 2010. Barrett, Julia, Ken R. Wells, and Jacqueline L. Longe. “Pain. (Disease/Disorder overview).” The Gale Encyclopedia of Medicine. Jan. 1, 2008. Gale. Academic OneFile. Web. 31 Jan. 2010. < http://find.galegroup.com/gtx/start.do?prodId=AONE&userGroupName=ntn >. Brownstein, M. J. “A brief history of opiates, opioid peptides, and opioid receptors.” Proc. Natl. Acad. Sci. USA . Vol. 90, pp. 5391-5393, June 1993. < http://www.ncbi.nlm.nih.gov/pmc/articles/PMC46725/pdf/pnas01469-0022.pdf >. 2 Feb. 2010. Calandra, Bob M. “Feeling your pain.” MedicineNet.com . Aug. 27, 2002. < http://www.medicinenet.com/script/main/art.asp?articlekey=51160 >. 3 Feb. 2010. Chudler, Eric H. Neuroscience for Kids: Conduction Velocity . 2008. < http://faculty.washington.edu/chudler/cv.html >. 31 Jan. 2010. Chudler, Eric H. Pain and Why It Hurts. < http://faculty.washington.edu/chudler/pain.html >.31 Jan. 2010. “ CIPA.” Sick Du Jour . March 19, 2009. < http://sickdujour.blogspot.com/search?updated‑max=2009‑03‑20T08%3A50%3A00‑04%3A00&m ax‑results=4 >. 3 Feb. 2010. “ Congenital Insensitivity to Pain with Anhidrosis.” Science Online . < http://www.scionline.org/index.php/Congenial_Insensitivity_to_Pain_with_Anhidrosis >. 30 May 2009. Connors, Barry W., Mark F. Bear, and Michael Paradiso. Neuroscience Exploring the Brain 2nd Edition B01_0829 . Maryland: Lippincott Williams & Wilkins, 2001. Print. Craig, A. D. (Bud). “Mapping pain in the brain.” The Wellcome Trust. < http://www.wellcome.ac.uk/en/pain/microsite/science2.html >. 2 Feb. 2009.
42. Dray, A. “Mechanisms of action of capsaicin-like molecules on sensory neurons.” Life Sci. 1992;51(23):1759-65. < http://www.ncbi.nlm.nih.gov/pubmed/1331641 >. Fields, Howard L. “Pain Perception—The Dana Guide.” The Dana Foundation. Nov. 2007. < http://www.dana.org/news/brainhealth/detail.aspx?id=10072 >. 2 Feb. 2010. Fisher, Brian D, Ph.D. “NSAIDs Case Analysis: New Approaches to Soft Tissue Injuries.” NSAIDs . July 7, 1999. < http://www.nsaids.com />. 3 Feb. 2010. Freudenrich, Ph.D., Craig. "How Pain Works." Nov. 9, 2007. HowStuffWorks.com. < http://health.howstuffworks.com/pain.htm >. 3 Feb. 2010. “ Gender and Pain.” Society for Neuroscience. May 2007. < http://www.sfn.org/index.aspx?pagename=brainBriefings_Gender_and_Pain >. 3 Feb. 2010. Gray, Peter O. Psychology, Fourth Edition. null ed. New York: Worth Publishers, 2002. Print. Holzer, Peter. “Neural Injury, Repair, and Adaptation in the GI Tract, II. The elusive action of capsaicin on the vagus nerve.” Am J Physiol Gastrointest Liver Physiol July 1998: Vol. 275, Issue 1, G8-G13. Hopley, Laura and Jo van Schalkwyk. “Pain Physiology.” Oct. 24 2006. < http://www.anaesthetist.com/icu/pain/Findex.htm#pain3.htm >. 2 Feb. 2010. “ How you feel pain.” Mayo Clinic. Feb. 13, 2009. < http://www.mayoclinic.com/health/pain/PN00017 >. 3 Feb. 2010. Leeman, Susan E. “Substance P and Neurotensin: Discovery, Isolation, Chemical Characterization and Physiological Studies.” J. Exp. Biol. (1980), vol. 89. pp. 193-200. < http://jeb.biologists.org/cgi/reprint/89/1/193.pd >. 29 Jan. 2010. Luttrell, Andy. “The Neurology of Pain Perception: How the Brain Feels Pain with Nociception.” Oct. 28, 2009. < http://biology.suite101.com/article.cfm/the_neurology_of_pain_perception >. 2 Feb. 2010. Miranda, Claudia et al. “Novel Pathogenic Mechanisms of CIPA Genetic Disorders Unveiled by Functional Analysis of NTRK1/NGF Receptor Mutations.” JBC Papers in Press . < http://www.jbc.org/cgi/reprint/M110016200v1.pdf >. Manuscript M110016200 (Nov. 21, 2001).
43. “ Nerve Pain and Nerve Damage: Symptoms and Causes.” Brain & Nervous System Health Center; WebMD. Oct. 8, 2008 . < http://www.webmd.com/brain/nerve-pain-and-nerve-damage-symptoms-and-causes >. 3 Feb. 2010. "Neuroscience for Kids - Receptors." UW Faculty Web Server. < http://faculty.washington.edu/chudler/receptor.html >. 1 Feb. 2010. “ Neurotransmission.” The Merck Manuals Online Medical Library.” Nov. 2005. < http://www.merck.com/mmpe/sec16/ch207/ch207a.html >. 3 Feb. 2010. Oliviera, Carlos R. D. et al. “Spinal Anesthesia in a Patient with Congenital Insensitivity to Pain with Anhidrosis.” Pain Medicine . < http://www.anesthesia‑analgesia.org/cgi/content/full/104/6/1561104 >. (2007): 1561-2. “ Pain.” Jan. 12, 2009. < http://courses.washington.edu/conj/sensory/pain.htm >. 1 Feb. 2010. “ Pain.” Magill’s Encyclopedia of Social Science: Psychology Volume 3. Ed. Nancy A. Piotrowski, Ph.D. Pasadena: Salem Press, 2003. "Pain." Neuroscience For Kids. Web. < http://faculty.washington.edu/chudler/pain.html >. 2 Feb. 2010. “ Pain Perception.” Lewis & Clark College . < http://legacy.lclark.edu/~reiness/neurobiology/Lectures/Pain%20Perception.pdf >. 3 Feb. 2010. Pathways 4 Pain . Aug. 9, 2009. < http://relievepain.wordpress.com/2009/08/09/pathways-4-pain />. 2 Feb. 2010. “ Scientists Study Children Who Feel No Pain.” Feb. 20, 2007. Voice of America News . < http://www.voanews.com/specialenglish/archive/2007-02/2007-02-20-voa3.cfm?moddate=2007-02- 20 >. 2 Feb. 2010. Stucky, Cheryl L., Michael S. Gold, and Xu Zhang. “Mechanisms of Pain.” Proceedings of the National Academy of Sciences of the United States of America . Oct. 9, 2001. vol. 98, no. 21. pp. 11845-11846. < http://www.pnas.org/content/98/21/11845.full >. Woodrow, Kenneth D., M.D. et al. “Pain Tolerance: Differences According to Age, Sex and Race.” Psychosomatic Medicine , Vol. 34, No. 6 (November-December 1972). < http://www.psychosomaticmedicine.org/cgi/reprint/34/6/548.pdf >. 1 Feb. 2010.