Anmerkung: Intro -- Preface -- Contents -- Contributors -- Chapter 1: Assessment of Itch and Pain in Animal Models and Human Subjects -- 1.1 Introduction -- 1.2 Assessment of Itch in Animal Models and Human Subjects -- 1.2.1 Assessment of Itch in Animal Models -- 1.2.1.1 Assessment of Itch in the Nape of Mice -- 1.2.1.2 Assessment of Itch in the Cheek of Mice -- 1.2.1.3 Assessment of Itch in the Legs of Mice -- 1.2.1.4 Assessment of Itch in the Eyes of Mice -- 1.2.1.5 Assessment of Itch in the Rats -- 1.2.2 Assessment of Itch in Human Subjects -- 1.2.2.1 Assessment of Itch Intensity and Quality -- 1.2.2.2 Defining Histamine-Dependent Itch -- 1.2.2.3 Defining Histamine-Independent Itch -- 1.2.2.4 Human Surrogate Models of Itch -- Electrically Evoked Itch -- Mechanically Evoked Itch -- Proteinase-Activated Receptor 2/4 (PAR)-Mediated Itch -- Mas-Related G-Protein-Coupled Receptor-Mediated Itch -- 1.3 Assessment of Pain in Animal Models and Human Subjects -- 1.3.1 Assessment of Pain in Animal Models -- 1.3.1.1 Tests Based on Thermal Stimuli -- The Tail-Flick Test -- The Paw Withdrawal Test Using Radiant Heat -- The Hot Plate Test -- Tests Using Cold Stimuli -- 1.3.1.2 Tests Based on Mechanical Stimuli -- Randall and Selitto Test -- Pricking Pain Test -- Von Frey Test -- Electronic Von Frey Hair -- Q-tip Test -- 1.3.1.3 Tests Based on Spontaneous Pain-Related Behavior -- Spontaneous Foot Lifting, Biting, and Licking to Estimate the Spontaneous Pain of Rats -- Formalin Test -- 1.3.1.4 Tests Based on Limb Function -- Weight-Bearing Analysis Using Incapacitance Tester or CatWalk Setup -- Posture and Gait Analysis with Stainless Steel Cylinder -- Assessment of Spontaneous Mobility with Biotelemetry System or Activity Boxes -- 1.3.1.5 Tests Based on Pain Emotion and Memory -- Conditioned Place Paradigm -- Conditioned Place Aversion (CPA, Fear Based). , Conditioned Place Preference, CPP (Award Based) -- 1.3.2 Assessment of Pain in Human Subjects -- 1.3.2.1 Requirements for Human Subjects for the Measurement of Pain -- 1.3.2.2 Assessment of Pain in Human Subjects Using Capsaicin -- 1.4 Relationship Between Animal Models and Human Subjects -- 1.4.1 Similarities Between Animal Models and Human Subjects -- 1.4.2 Differences Between Animal Models and Human Subjects -- 1.5 Limitations of Animal Models and Human Subjects -- 1.5.1 Limitations of Animal Models -- 1.5.2 Limitations of Human Subjects -- 1.6 Conclusion -- References -- Chapter 2: Allergic Contact Dermatitis: A Model of Inflammatory Itch and Pain in Human and Mouse -- 2.1 Introduction -- 2.2 ACD Produced a Persistent Itch and Enhanced Stimulus-Evoked Itch and Nociceptive Sensations -- 2.3 ACD Enhanced Itch- and Pain-Like Behaviors in Mice -- 2.4 ACD Enhanced the Excitability of Cutaneous Mechanosensitive C-nociceptors in Mice -- 2.5 ACD Upregulates CXCR3 Chemokine Receptor Signaling in Cutaneous C-nociceptors -- References -- Chapter 3: Modulation of C-nociceptive Activities by Inputs from Myelinated Fibers -- 3.1 Introduction -- 3.2 A Rapid-Onset of Selective Demyelination of A-fibers by Cobra Venom Injection -- 3.3 A-fiber Demyelination Induced Neuropathic Pain and Inflammatory Responses -- 3.4 Cobra Venom Intra-Nerve Injection Induced Hyperexcitability of C-fiber Poly-Modal Nociceptors -- 3.5 Interruption of A-fiber Conductivity Evoked Antidromic Activity in C-fibers -- 3.6 Dorsal Root Reflexes (DRRs) Involve in Hyperexcitability of C-Fiber Nociceptors Induced by Demyelination of A-fibers -- References -- Chapter 4: New Mechanism of Bone Cancer Pain: Tumor Tissue-Derived Endogenous Formaldehyde Induced Bone Cancer Pain via TRPV1 Activation -- 4.1 Introduction -- 4.2 Formaldehyde Concentration Increased in Cancer Cells and Tissues. , 4.2.1 Formaldehyde Concentration Increased in Cultured MRMT-1 Cells -- 4.2.2 Formaldehyde Concentration Rose in Tumor Tissues from Cancer Patients -- 4.2.3 Formaldehyde Concentration Was Elevated in Tissues from Rats with Bone Cancer Pain -- 4.2.4 Formaldehyde Concentration Increased in Tumors and Sera of the MRMT-1 Subcutaneous Vaccination Rats -- 4.2.5 LSD1 in MRMT-1 Cells Participated in the Production of Endogenous Formaldehyde -- 4.2.5.1 LSD1 Protein Expression in Cancer Cells and Tissues -- 4.2.5.2 Inhibition of LSD1 Function Decreased Formaldehyde Concentration and Bone Cancer Pain -- 4.3 Formaldehyde Induced Bone Cancer Pain via TRPV1 Activation -- 4.3.1 Formaldehyde-Induced Bone Cancer Pain -- 4.3.1.1 Formaldehyde at Low Concentration Induced Acute Pain Behaviors -- 4.3.1.2 Formaldehyde Secreted by Cancer Tissues Induced Bone Destruction -- 4.3.1.3 Formaldehyde Enhanced Neural Excitatory -- 4.3.2 Formaldehyde Induced Pain Responses via TRPV1 -- 4.3.2.1 Formaldehyde Increased TRPV1 Expression in Primary Cultured DRG Neurons -- 4.3.2.2 Inhibitory Effects of MAPK and PI3K Inhibitors on Formaldehyde-Induced TRPV1 Upregulation in Primary Cultured DRG Neurons -- 4.3.2.3 Formaldehyde Induced Ca2+ Influx and Elicited Currents in TRPV1-CHO Cells with pH of 6.0 -- 4.3.2.4 Formaldehyde Induced Pain Behaviors via TRPV1 Activation -- 4.4 IGF-1 Enhanced TRPV1 Function in Bone Cancer Pain (Li et al. 2014) -- 4.4.1 IGF-1 Expression Increased in MRMT-1 Bone Cancer Pain Rats -- 4.4.2 TRPV1 Current Density and Protein Expression Increased in DRG Neurons in MRMT-1 Bone Cancer Pain Rats -- 4.4.3 TRPV1 Expression Increased as Well as Functionally Enhanced in Bone Cancer Pain Rats -- 4.4.3.1 Co-localization of IGF-1 Receptor and TRPV1 in DRG Neurons -- 4.4.3.2 IGF-1 Incubation Increased Total and Membrane TRPV1 Protein Expression in Primary Cultured DRG Neurons. , 4.4.3.3 IGF-1 Incubation Increased TRPV1 Current Density in Primary Cultured DRG Neurons -- 4.4.4 IGF-1R Inhibitor Reversed Pain Behavior in Bone Cancer Pain Rats -- 4.5 Conclusion -- References -- Chapter 5: Neuropathic Pain: Sensory Nerve Injury or Motor Nerve Injury? -- 5.1 Introduction -- 5.2 Injury to Motor Fibers But Not to Sensory Fibers Often Induces Lasting Allodynia and Hyperalgesia -- 5.2.1 The Differential Effects of Injury to Motor Fibers and Sensory Fibers on Peripheral Sensitization -- 5.2.2 The Ectopic Discharges in Intact But Not in Injured Afferents Are Responsible for Neuropathic Pain -- 5.2.3 The Ectopic Discharge Is Produced by Injury to Motor Fibers But Not to Sensory Fibers -- 5.2.4 The Differential Effects of Motor Fiber Injury and Sensory Fiber Injury for the Expression of Voltage-­Gated Sodium Channels in Dorsal Root Ganglion Neurons -- 5.3 The Differential Effects of Injury to or Electrical Stimulation of Motor Fibers and Sensory Fibers on Central Sensitization -- 5.3.1 Activation of Muscle Afferents But Not Skin Afferents Induces Late-Phase LTP in Spinal Dorsal Horn -- 5.3.2 Injury to Motor Fibers May Induce Spinal LTP at C-Fiber Synapses, Indirectly -- 5.4 The Motor Fiber Injury Leads to the Neuropathic Pain by Upregulation of Pro-inflammatory in Pain Pathway -- 5.4.1 Nav1.3 and Nav1.8 in DRG Neurons Are Upregulated by TNF-α But Downregulated by IL-10 -- 5.4.2 TNF-α and BDNF Are Essential for Induction of Spinal LTP at C-Fiber Synapses -- 5.4.3 The Direction of Synaptic Plasticity at C-Fiber in Spinal Dorsal Horn Is Decided by Microglia -- 5.5 Concluding Remarks -- References -- Chapter 6: Peripheral Nociceptors as Immune Sensors in the Development of Pain and Itch -- 6.1 Introduction -- 6.2 Morphological Correlations Between the Peripheral Nervous System and the Immune System. , 6.3 Interactions Between the Peripheral Nervous and the Immune System -- 6.4 The Immune-Related Receptors in Peripheral Nociceptors -- 6.5 Conclusion -- References -- Chapter 7: Mas-Related G Protein-Coupled Receptors Offer Potential New Targets for Pain Therapy -- 7.1 History of the Mas-Related G-Protein-Coupled Receptor (Mrgpr) Family -- 7.2 Distribution of Mrgpr -- 7.3 Mrgpr Receptors: Potential Pain Modulators -- 7.4 Mrgpr A and D -- 7.5 MrgprB -- 7.6 MrgprC -- 7.6.1 Facilitation of Pain by MrgprC in Rodents -- 7.6.2 Role of MrgprC in Pain Inhibition in Rodents -- 7.7 MrgprE-H -- 7.8 MrgprX1 -- 7.9 MrgprX2 -- 7.10 MrgprX3 and 4 -- 7.11 Conclusions and Future Directions -- References -- Chapter 8: Pain Modulation and the Transition from Acute to Chronic Pain -- 8.1 Introduction -- 8.2 The PAG and RVM as a Pain-Modulating Circuit -- 8.3 Is Pain Modulation a Specific Function of the PAG-RVM System? -- 8.4 Inputs to the PAG-RVM Pain-Modulating System -- 8.5 RVM Plasticity in Persistent and Chronic Pain -- 8.6 Conclusions -- References -- Chapter 9: Advances in the Treatment of Neuropathic Pain -- 9.1 Introduction -- 9.2 Pharmacological Treatment -- 9.3 Nonpharmacological Treatment -- 9.4 The Treatment of Common Neuropathic Pain -- 9.4.1 Central Pain -- 9.4.2 Peripheral Pain -- 9.4.3 Cancer Pain -- 9.5 Conclusion -- References -- Chapter 10: Integrated, Team-Based Chronic Pain Management: Bridges from Theory and Research to High Quality Patient Care -- 10.1 Pain Prevalence -- 10.2 Defining Chronic Pain -- 10.3 Goals of Chronic Pain Treatment -- 10.4 Core Principles for Effective Pain Management -- 10.4.1 Empathy -- 10.4.2 Biopsychosocial Assessment -- 10.4.3 Manage Expectations/Set Functional Goals -- 10.4.4 Partner with Patients to Make Shared Medical Decisions -- 10.4.5 Utilization of Targeted, Rational Polypharmacy. , 10.4.6 Employ Multidisciplinary Treatment Plan.