NYERI
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Nyeri merupakan pengalaman sensorik dan emosional yang tidak menyenangkan yang terkait dengan kerusakan jaringan, baik aktual maupun potensial. Nyeri berperan melindungi tubuh dan merupakan mekanisme pertahanan. Terdapat dua jenis nyeri yaitu nyeri cepat yang tajam dan nyeri lambat yang menyiksa dan bersifat kronis.
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NYERI
- 2. Nyeri adalah pengalaman sensorik dan emosional yang tidak menyenangkan terkait kerusakan jaringan, baik aktual maupun potensial atau yang digambarkan dalam bentuk kerusakan tersebut.
- 3. Nyeri adalah anugerah “Pain is alarm protection tell us that something wrong in our body”. Sulit dibayangkan seandainya tubuh kita tidak dilengkapi dgn “reseptor nyeri”, sehingga kita tidak pernah menyadari kalau tubuh kita telah terancam kerusakan.
- 4. Pain can occur due toPain can occur due to Potential tissue damage --- > Physiological Pain Actual tissue damage ----- >Actual tissue damage ----- > NociceptiveNociceptive pain or Acute pain or inflammation painpain or Acute pain or inflammation pain Described in term of such damage ----- >Described in term of such damage ----- > Chronic PainChronic Pain
- 5. Pain that occur to stimulate withdrawalsPain that occur to stimulate withdrawals reflexreflex To prevent tissue damageTo prevent tissue damage To prevent our body from hatmful things.To prevent our body from hatmful things.
- 6. Acute Pain or Nociceptive Pain is pain thatAcute Pain or Nociceptive Pain is pain that elicited by activation of nociceptorselicited by activation of nociceptors There are 4 distinct process involved:There are 4 distinct process involved: 1. Transduction1. Transduction 2. Transmission2. Transmission 3. Modulation and3. Modulation and 4. Perception4. Perception
- 7. Pain Perception Brain Dorsal Root Ganglion Dorsal Horn Nociceptor Spinal Cord Gottschalk A et al. Am Fam Physician. 2001;63:1979-84. Fields HL et al. Harrison’s Principles of Internal Medicine. 1998:53-8.
- 8. 1. Transduction Conversion of noxious stimuli (mechanical, thermal, chemical into electrical activation 2 Transmission Communication of the nerve impulse from the periphery to the spinal cord, up to spinothalamic track to the thalamus and cerebral cortex 3 Modulation Process by which impulse travel from the brain back down to the spinal cord to selectiveley inhibit (or sometimes amlpify) pain impulse 4 Perception Net result of three events – the subjective experience of pain
- 9. Pain perception much depend onPain perception much depend on modulation ---- > 3 possibilitiesmodulation ---- > 3 possibilities 1.1.Nociception without painNociception without pain (ada n(ada nosisepsi tanpa nyeri)osisepsi tanpa nyeri) 2.2.Nociception with painNociception with pain (ada nosisepsi dengan nyeri).(ada nosisepsi dengan nyeri). 3.3.Pain without NociceptionPain without Nociception (ada nyeri tanpa nosisepsi)(ada nyeri tanpa nosisepsi)
- 11. The Somatosensory System Somatosensory cortex Thalamus Hypothalamus Ascending tracts Midbrain Medulla Spinal cord Frontal cortex Descending pathway Periaqueductal gray matter Dorsal horn area Noxious stimuli activate receptors in periphery
- 12. Activation of the Central Nervous System at the Spinal Cord Level Tissue Damage Activation of the Peripheral Nervous System Transmission of the Pain Signal to the Brain Pain Samad TA et al. Nature. 2001;410:471-5.
- 13. Nyeri dibedakan atas: Nyeri Neuropatik: Nyeri yang disebabkan oleh lesi (kerusakan) sistem saraf. Nyeri Nosiseptif: Nyeri yang disebabkan oleh proses inflamasi dan kerusakan jaringan
- 14. Pd keadaan sakit, tubuh merasakan nyeri Nyeri merupakan mekanisme pertahanan tubuh sehingga individu memindahkan stimulus nyeri Ada 2 jenis rasa nyeri: ☼ Nyeri cepat: tajam, menusuk, rasa kesetrum dan akut. ☼ Nyeri lambat: rasa terbakar, pegal, berdenyut, nyeri mual dan khronik
- 15. VR1 Extern al Stimuli Adapted from Woolf CJ et al. Science. 2000;288:1766. •Heat •Chemical •Mechanical Voltage-Gated Sodium Channels Action Potentials Ca2+
- 16. Reseptor nyeri dan rangsangannya: Semua reseptor adalah ujung saraf bebas. Tersebar dipermukaan kulit dan jaringan seperti: - periosteum - dinding dalam arteri - permukaan sendi - falks / tentorium serebri Ada 3 macam stimulus: - mekanik - suhu - kimiawi
- 17. VR1 BK Recept or HEAT External Stimulus Sensitizing Stimulus PGE 2 Bradykinin PK A PKCε EP Recept or SNS/PN3SNS/PN3 TTX-ResistantTTX-Resistant SodiumSodium ChannelChannel Adapted from Woolf CJ et al. Science. 2000;288:1766.EP = prostaglandin E; BK = bradykinin.
- 18. Nyeri berperan melindungi tubuh Nosiseptor adalah suatu reseptor nyeri pada ujung saraf bebas yg ditemukan pada jaringan tubuh, kecuali otak. Rangsangan termal, kimia dan mekanik akan mengaktifkan nosiseptor, dengan jalan melepaskan prostaglandin, kinin dan ion kalium
- 19. ☻Impuls nyeri cepat - berlangsung cepat (0,1 dtk pasca rangsangan - disepanjang saraf tipe A bermielin - nyeri bersifat akut, tajam atau menusuk - tdk dijumpai pd struktur dalam
- 20. ☻ Impuls nyeri lambat terjadi disepanjang saraf tipe C tdk bermielin - nyeri sangat menyiksa, dan menjadi khronik spt; rasa terbakar, tumpul dan berdenyut. spt sakit gigi dan infeksi kuku, - nyeri pd rangsangan reseptor kulit disebut dgn; superficial somatic pain - pd rangsangan otot skeletal, sendi, tendon disebut; deep somatic pain
- 21. - nyeri viseral; akibat rangsangan nosiseptor organ pd viseral spt distensi abdomen dan iskhemia organ internal. - zat kimia yg merangsang nyeri adalah bradikinin, serotonin, ion kalium, asetil kholine dan enzim proteolitik
- 22. Dua jaras penyaluran sinyal nyeri ke sistem saraf pusat ☻Nyeri cepat dan tajam dirangsang oleh mekanik dan suhu. - disalurkan ke medula spinalis oleh serabut tipe Aδ - kecepatan 6-10 m/detik. ☻Nyeri lambat dirangsang secara kimia, mekanik dan suhu - disalurkan melalui saraf tipe C - kecepatan 0,5-2 m/dtk
- 23. Dorsal Horn Dorsal root ganglion Peripheral sensory Nerve fibers Aβ Aδ C Large fibers Small fibers There are Two Sensory Afferent Neurons 1. Large myelinated Aβ fibers, very fast conduction velocity. Respond to innocuous stimuli 2. Small myelinated Aδ & C unmyelinated fibers, have slow conduction velocity. Respond to noxious stimuli
- 24. DHN PAIN INNOCUOUS SENSATION NOXIOUS STIMULUS INNOCUOUS STIMULUS DHN Touch Tactile Pressure Physiological Pain Aδ C fiber Aβ First Pain Second Pain
- 25. Dari kornu dorsalis menuju otak, sinyal nyeri disalurkan di MS melalui: ☻Tr. Neo-spinotalamikus - untuk nyeri cepat berakhir di lamina I (lamina marginalis) – kolumna anterolat. - sebgn berakhir di kompleks ventrobasal dan sebgn lagi di korteks somatosensorik
- 26. ☻Tr. Paleo-spinotalamikus - utk nyeri lambat dan khronik melalui saraf tipe C dan sebgn saraf tipe Aδ - berakhir di lamina II dan III subs. Gelatinosa dan lamina V dan VII kornu dorsalis - Neurotransmiternya Subst. P dan Glutamat - Berakhir di tiga tempat ■ Nc. Retikularis medula, pons dan mesensefalon ■ Area tekt. mesensefalon dan kol. Sup dan Inf ■ Subst. grisea peri akuadukt
- 27. Dorsal Horn Neuron C-Fiber Terminal AMPA NMD A Ca2+ Glutamate PKC P P (+) (+) (-) Woolf CJ et al. Science. 2000;288:1765-8. Schwartzman RJ et al. Arch Neurol. 2001;58:1547-50. Substance P
- 28. DHN GATE CONTROL SYSTEM ++ ++ ACTIONACTION SYSTEMSYSTEM Brain SG + - -- -- Aβ C 1965 MELZACK and WALL1965 MELZACK and WALL Introduce Hypothesis ofIntroduce Hypothesis of ““GATE CONTROL THEORY”GATE CONTROL THEORY” The beginning of “MODULATION”
- 29. Reaksi seseorang terhadap nyeri bervariasi. Dipengaruhi otak melakukan inhibisi (sistem analgesia). Ada 3 komponen: 1. Area periakuadukt grisea dan periventr. mesensefalon., sinyal dikirim ke 2. Nukl. Raphe magnus dibawah pons diatas medula obl. Dan disalurkan ke 3. Kompleks penghambat rasa nyeri radiks dorsalis MS kemudian dipancarkan ke-otak
- 30. Enkefalin disekresikan oleh nc. periventrik, area peri akuadukt dan raphe magnus. menghambat pd pre dan post sinaps serabut nyeri tipe C dan Aδ Serotonin oleh radiks dorsalis MS menghambat pd pre-sinaptik terhadap ion kasium.
- 31. Sistim Opium Otak, Endorfin dan Enkefalin ☻Morphin like subst. bekerja pd sebagian sistem analgesia. Ada 12 macam opium like subst di-otak Berasal dari pemecahan 3 mol. Protein, y.i pro- opiomelanokortin, pro-enkefalin dan pro- dinorfin. Bhn yg penting adalah β-endorfin, met- enkefalin dan leu-endorfin.
- 32. Pd reseptor sensasi diseleksi dan di-olah jadi 4 tahap 1. Rangsangan reseptor sensorik - Hrs tepat dan adekuat hingga terjadi respons. 2. Transduksi stimulus. - terjadi pd kornu dorsalis MS (dikonversi) menjadi energi rangsangan (gradasi pot tergantung kuat rangsangan dan ampl
- 33. 3. Membangkitkan impuls saraf. - Pd grad. potensial mencapai ambang tercetus 1 impuls atau lebih, kmdian menyebar ke pusat. 4. Integrasi input sensorik. Daerah tertentu di-otak akan menerima dan meng-integrasikan impuls sensorik dan diterima pd area tertentu di korteks
Editor's Notes
- Activation of peripheral pain receptors, also called nociceptors, by noxious stimuli generates signals that travel to the dorsal horn of the spinal cord via the dorsal root ganglion. From the dorsal horn, the signals are carried along the ascending pain pathway or the spinothalamic tract to the thalamus and the cortex. Pain can be controlled by pain-inhibiting and pain-facilitating neurons. Descending signals originating in supraspinal centers can modulate activity in the dorsal horn by controlling spinal pain transmission.1,2 Gottschalk A, Smith DS. New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician. 2001;63:1979-1984. Fields HL, Martin JB. Pain: pathophysiology and management. In: Fauci AS, Braunwald E, Isselbacher KF, et al, eds. Harrison’s Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:53-58.
- <<Animated slide: Please advance to view entire sequence.>> The pain response is a complex process that involves both the peripheral nervous system (PNS) and the central nervous system (CNS). Tissue injury results in the activation of the PNS. Signals from the PNS travel into the CNS. They move through the spinal cord before traveling to the brain, where pain perception occurs. In addition, pain perception can be transmitted directly from the site of injury to the CNS via a humoral signal (probably via interleukin [IL]-6), which then induces cyclooxygenase (COX)-2 in the CNS.1 This concept will be discussed in greater detail later in the presentation. Samad TA, Moore KA, Sapirstein A, et al. Interleukin-1-mediated induction of COX-2 in the CNS contributes to inflammatory pain hypersensitivity. Nature. 2001;410:471-475.
- Transducer receptor/ion channel complexes on peripheral nociceptor terminals respond to noxious stimuli from mechanical, chemical, or heat sources by generating depolarizing currents. If the current is sufficient, action potentials are initiated and then conducted to the CNS, where they invade central nociceptor terminals and cause the release of neurotransmitters, thus eliciting pain perception. Depicted here is the activation of vanilloid receptor VR1 by noxious heat stimuli, resulting in the generation of action potentials that travel to the spinal cord to cause the release of transmitters.1 Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288:1765-1768.
- Modulation is a result of receptor/ion channel phosphorylation, which causes a change in the expression of channels on the surface of primary sensory neurons. Sensitizing agents such as prostaglandin E2 (PGE2) and bradykinin released during tissue damage or by inflammatory cells sensitize nociceptor terminals. Nociceptors undergo modulation as a result of simultaneous activation of the intracellular kinase protein kinase A (PKA) or protein kinase C (PKC), the phosphorylation of a tetrodotoxin (TTX)-resistant sensory neuron–specific sodium ion channel (SNS; also referred to as SNS/PN3), and possibly the phosphorylation of VR1. Phosphorylation of SNS channels causes an influx of sodium ions. Consequently, the excitability of nociceptor terminal membranes increases, and peripheral nociceptors become more sensitive to subsequent stimuli.1 Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288:1765-1768.
- Following mild noxious stimuli, dorsal horn neurons are activated primarily by fast excitatory postsynaptic potentials (EPSPs) produced by unmyelinated nociceptive C-fibers. These fast EPSPs signal the onset, duration, intensity, and location of the stimulus. More intense stimuli generate higher frequency inputs and cause the synaptic release of glutamate and other neuromodulators, such as substance P, from the C-fibers to act on alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). This produces slow EPSPs lasting tens of seconds.1 Repeated stimulation allows for temporal summation of slow EPSPs, resulting in the removal of the magnesium blockade on N-methyl D-aspartate (NMDA) channels.1 The increased current through the NMDA channels enhances the cumulative depolarization caused by slow EPSPs. The result is a “windup” of action potential discharge on central pain-projecting neurons and neuronal modulation.1,2 Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288:1765-1768. Schwartzman RJ, Grothusen J, Kiefer TR, et al. Neuropathic central pain: epidemiology, etiology, and treatment options. Arch Neurol. 2001;58:1547-1550.