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Pain pathway
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- 2. CONTENTS •Introduction •Characteristics of pain •Typesof pain sensation •Gate control Hypothesis •Difference b/w sometic & visceral sensory function •Visceral pain & referred pain •Receptors & Sensations
- 3. •Pathway of sensoryimpulses •Tooth pulp pain •Applied physiology •Management •Conclusion •References
- 4. INTRODUCTION Unpleasant sensory &emotional experience associated with actual or potential tissue damage. Its imp: , symptoms of many diseases & when pt experiences pain he/she consults a physician.
- 5. Characteristics • specific withspecific receptors & afferent fibers. •Less adaptation & continues as long as pain causing agent persists. •Chronic pain- psychological effects. •Tolerance level varies from individuals. •Cerebral cortex – localization, discrimination & interpretation.
- 6. Types of painsensation 1) Fast pain- short & sharp conducted by Aδ fibers localization of pain is better 2) Slow pain- more prolonged & severe conducted by C fibers dull, diffused & localization is poor 3) Deep pain- contraction of skeletal muscles when pain is severe, causes sweating, nausea & vomiting, fall in B.P
- 7. Aδ – fast,sensitive to mechanical noxious stimuli. small, myelinated. High conductance speed C – slow, sensitive to many noxious stimuli (chemical, etc.) – small, unmyelinated. Slow conductance speed
- 8. Receptors They are specializedafferent nerve endings designed to respond appropriate & adequate stimulus. Function Converts various forms of energy into action potential in nerve fibers Act as transducers Situated at various parts of body- skin, eye, ear, nose, muscle etc
- 9. Properties Excitability – specificity receptiveresponse Adaptation Effect of extend of stimulus Localization & projection Effect of strength of stimulus Quality or modality of sensation Intensity of sensation Fatigue
- 10. Classification •Exteroreceptors- responds tochange in external enviornment a) cutaneous receptors- touch, pain, temp: b) chemical receptors- taste & smell c) teleceptors- vision & hearing
- 11. •Interoceptors – exitedby stimuli within the body a) Stretch receptors- alvoeli of lungs b) Chemoreceptors- aortic & carotid bodies c) baroreceptors- carotid sinus & aortic arch d) Osmoreceptors- hypothalamus e) Volumereceptors- right atrium f) Proprioreceptors- muscle spindle, tendon g) Visceroreceptors- present in visera
- 12. Nociceptors are special receptorsthat respond only to noxious stimuli and generate nerve impulses which the brain interprets as “pain”.
- 13. 1. Prevents seriousdamage. 2. Teaches one what to avoid 3. If pain is in joints, pain limits the activity, so no permanent damage can occur. but pain can become the problem, and cause people to want to die. Purpose of pain
- 14. Differences btw Somatic& Visceral sensory function. Somatic :- seen on skin & subcutaneous tissues subserve sensory function of touch, temp,sensation, pressure & pain Visceral:- have no proprioreceptors & sparesly distributed subserve osmorecptors, barorecptors
- 15. PAIN STIMULI 3 types-thermal, mechanical & chemical. Nociceptive stimuli- stimuli which threatens the welfare of tissues & causes pain. Chemical substances that can induce pain intrinsic- bradykinin, histamine, prostaglandins extrinsic- irritant acid, alkali, plant & animal stings & venoms
- 16. 1. gray matter 2.white matter 3. gray commissure 4. central canal Dorsal and ventral nerve roots Internal Anatomy
- 17. Tracts of theSpinal Cord
- 18. Cross section ofspinal cord , showing ascending tracts & descending tracts
- 19. Three major pathwayscarry sensory information Posterior column pathway (gracile & cuneate fasciculi) Anterolateral pathway (spinothalamic) Spinocerebellar pathway
- 20. THREE neurons fromthe receptor to the cerebral cortex First order neuron: Cell body located in the dorsal root ganglion. The Axon passes to the spinal cord through the dorsal root of spinal nerve, runs ipsilaterally and synapses with second-order neurons in the cord and medulla oblongata
- 21. Second order neuron: Hascell body in the spinal cord or medulla oblongata & Terminate on 3rd order neuron Third order neuron: Has cell body in thalamus Axon terminates on cerebral cortex ipsilaterally
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- 24. PAIN IMPULSE PATHWAY Ventral spinocerebellar Dorsal spinocerebellar (1storder neuron) (2nd order neuron) (3rd order neuron) Lateral corticospinal
- 25. Pain Free nerve ending Posterior nerve rootganglion Fibers from lateral spinothalamic tract Ventral posterolateral nucleus of thalamus, reticular formation & midbrain. Sensory cortex Receptor First order neuron Second order neuron Third order neuron center
- 26. Tissue ischemia Blood flowis blocked for few min- pain Results in anaerobic metabolism & release of bradykinin & proteolytic enzymes- cell damage
- 27. Muscle spasm Indirect effectmuscle spasm to compress the blood vessels & cause ischemia Results – release of chemicals and increase in metabolism in muscle tissue.
- 28. Visceral pain They aredull & diffuse, poorly localized, and associated with symptoms like nausea & referred to other areas Stimuli for visceral pain ischemia, obstruction, spasm, chemical stimuli.
- 29. REFERRED PAIN FROMVISCERAL ORGANS Referred pain Pain felt in a part of the body that is fairly remote from tissue causing pain. Pain at diaphragm is felt over tip of shoulder Pain at maxillary sinus felt at nearby teeth. A tooth abscess can cause jaw bone pain.
- 30. Convergence theory bothsomatic & visceral afferent fibers converge upon 2nd order neuron Somatic fibers conduct impulses more frequent. Visceral pain is felt as somatic pain because brain is familiar with somatic regions.
- 31. Facilitation theory Visceral &somatic fiber join at adjoining spinothalamic neurons( 2nd order neurons) When strong impulses conduct, activation of spinothalamic neurons, resulting in impulses passing through spinothalamic pathway This results in misinterpretation in location of pain.
- 32. Melzack & Waller-1965 Pain impulses in spinal cord can be modified by other afferent impulses entering the spinal cord with posterior horn acting as gate Gate control hypothesis/ gate theory of pain
- 33. Gate open Gateclosed Physiological Aδ and C fibers active, Overuse, Fatigue , improper mechanics, tired Aδ or Aα active, Relaxation, exercise, strengthening/ conditioning Medical Extent of injury/pathological condition Medication, cooling/heating Congenitive Focusing on pain, anxiety , fear, depression, stress Distraction, relaxation, happiness, positive attitude
- 34. Tooth pulp pain 1)Exposure of dentinal tubules elicit toothache & other non noxious sensation. 2) Both Aδ & C fibers respond to stimuli in dentine 3) Transmission of stimuli across dentin, mediated by movement of fluid through odontoblast tubules.
- 35. 4) Fibers terminateat medullary dorsal horn & synapse and also at trigeminal sensory nucleus 5) From trigeminal nucleus send inf: thalamus & sensory cortex 6) Pulpal innervation are capable of regenerating & reinnervating
- 36. Determinants of painfulexperience during dental treatment Pain occurs due to invasive procedures like extractions & surgeries or non invasive procedures. With regard to children, studies have shown that dentists do not believe in pain referred by children & tend not to use available methods to control pain. Conclusion: anxiety is determinant for pain during dental care & pain is related to local anesthetic procedures. There are evidences that dentists attitude are determinants for pain. Ruth et al Rev.dor; 2012; 13(4)
- 37. Pain assessment visualanalogue scale
- 39. The sensory functionsare affected by lesions in sensory pathways or other nervous disorders. 1) Anesthesia – loss of sensation 2) Hyperesthesia- increase sensitivity to sensory stimuli 3) Hypoesthesia- decrease sensitivity to sensory stimuli 4) Hemiesthesia – loss of sensation to one part of body 5) Paresthesia- abnormal sensation
- 40. 6) Dissociated anesthesia-loss of some sensation with loss of consciousness produced by anesthetic agents 7) General anesthesia- loss of all sensation with loss of conciousness produced by anesthetic agents 8) Local anesthesia- loss of sensation restricted area of body 9) Tactile anesthesia- loss of tactile sensation
- 41. 10) Hyperaglasia-increase insensitivity to pain 11) Paraglesia- abnormal pain sensation 12) Thermic anesthesia- loss of thermal sensation 13) Pallanesthesia- loss of sensation of vibration 14) Analgesia- loss of pain sensation
- 42. Herpes zoster- viralinfection affecting dorsal root ganglion. Results in severe pain which facilitates the pain towards the ganglion.
- 43. Tic Doulourex Pain feltat one side of the face Felt like sudden electric shock, may last for secs or may be continous Corrected by surgery at hypersensitive area
- 44. Brown-Sequard syndrome All sensationsare blocked at one side Sensations like pain, heat & cold, vibrations are blocked
- 45. In a studyby Pornachi et al- A case reported on a 63yr old woman with Brown-Sequard Syndrome due to spontaneous C5-C6 cervical disc herniation. Anterior discectomy was performed with favorable outcome. Neurology Asia .2007;12;65-67
- 46. Management NSAIDs – paracetamol,capsacin L.A- reduces pain Opoids- Anticonvulsants- interferes with Na & Ca channel function
- 47. Conclusion Pain can inducephysiological & anatomical changes within the nervous system. The complexity of pain transmission means there are many pharmological targets & multimodel therapy is required to optimize pain control.
- 48. References Essential of oralphysiology- Robert M Bradley Textbook of medical physiology- Guyton & Hall Essential of medical physiology- K.Sembulingam & Prema Sembulingam Textbook of human physiology- S Chand Articles •Determinants of painful experience during dental treatment- Ruth Suzanne et al Rev.Dor 2012;13(4) •Case report study on Brown sequard syndrome- Ponachi et al Neurology Asia 2007;12;65-67 •Anatomy, physiology & pharmacology of pain- Ryan Moffat, Colin P.Rae anesthesia & intensive care medicine; 2010;12(1)