Pain pathways

This ppt shows about components of pain transmission and its pathways

1. Pain pathways Dr.L Vasavi reddy I MDS

2. CONTENTS Introduction Definition History Incidence Classification Theories of pain pathways Components of pain transmission Neural pain pathways Pain pathways Genes involved in pain transmission Applied aspects Management of pain

3. INTRODUCTION: Pain and fear of pain continue to be strongest motivation of patient to seek dental care The head and face are subjected to chronic persistent or recurrent pain more often than any other part of the body Therefore, the dentist responsibility in managing the pain is two fold, first is the diagnosis and second is therapy for which knowledge on pain pathways is essential

4. HISTORY The word pain is derived from ‘ poine ’ meaning penalty or payment, which certain religious segments have translated it s synonyms for punishment Homer thought that pain was result of arrows shot by god Aristotle was the first to distinguish five physical senses considering “pain as passion of soul” Plato described pain as emotional experience more than a localized body disturbance John Bonica - father of pain

5. DEFINITIONS Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage( by International Association for Study of Pain ) An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such ( Monheim )

6. classification

7. According to temporal relation and duration

8. According to qualities of pain

9. According to pain localization

10. Fast pain is felt within about 0.1 second after a pain stimulus is applied. It is also described by many alternative names, such as sharp pain, pricking pain, acute pain, and electric pain.   Slow pain begins only after 1 second or more and then increases slowly over many seconds and sometimes even minutes. Slow pain also goes by many names, such as slow burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain. Slow pain Fast pain

11. Theories of pain Specificity Theory of Pain: Each modality (touch and pain) is encoded in separate pathways. Intensive Theory ( Erb , 1874) Rather, the number of impulses in neurons determines the intensity of a stimulus.

12. Pattern Theory of Pain posits that somatic sense organs respond to a dynamic range of stimulus intensities. Gate Control Theory of Pain proposes that both large (A-fibers) and small (C-fibers) synpase onto cells in the substantia gelatinosa (SG) and the 1st central transmission (T) cells.

13. Other theories:

14. Levels of pain processing

15. Components of pain transmission

16. Sensory Receptors At distal terminals of afferent nerves are specialized sensory receptors that respond to physical or chemical stimuli. When they are adequately stimulated, impulse is generated in primary afferent neuron which is carried centrally to CNS They are classified as: Exteroceptors Proprioceptors interoceptors

17. Merkels corpuscles Meissner’s corpuscles Ruffini’s corpuscles Krause’s corpuscles Free nerve endings Muscle spindles Golgi tendon organs Pacinian corpuscles Periodontal mechano receptors Free nerve endings Pacinian corpuscles Free nerve endings

18. Nociceptors Nociceptors are receptors in tissues which are activated specifically by painful stimuli. The tissue area for which the nociceptor is responsible is receptive field. This ‘noxious’ information is transduced by the receptors into an electrical signal and transmitted from the periphery to the central nervous system along axons. There are two types of nociceptors: A) high-threshold mechanoreceptors (HTM), which respond to mechanical deformation B) polymodal nociceptors (PMN), which respond to a variety of tissue-damaging inputs: hydrogen ions (protons) 5-hydoxytryptamine (5-HT) cytokines bradykinin histamine prostaglandin Nociceptors are the free nerve endings of nerve fibres .

19. Neurons Nerve fibers can be classified based on different criteria: Depending on number of axons present, unipolar, bipolar or multipolar Histologically, as myelinated or non-myelinated Functionally, as afferent (sensory) or efferent (motor). Based on diameter and conduction velocity which is known as Gasser and Erlanger’s classification. Based on the type of neurotransmitter released from their terminals as adrenergic, cholinergic, dopaminergic, etc.

20. First order neurons: these are primary afferent neurons attached to sensory receptors that carry impulses to CNS They are three types of afferents: mechanothermal ( A delta), high threshold meachano receptive (A delta), polymodal(c fibres ) Second order neurons: these are transmission neurons There are three types of second-order neurons in the dorsal horn: nociceptive specific (NS) - respond selectively to high-threshold noxious stimuli - found in laminae II and III wide dynamic range (WDR) - respond to a range of sensory stimuli - found in laminae V and VI low-threshold (LR) - respond solely to innocuous stimuli. Third order neurons: Third order neurons are in the subcortical areas. Fibers of these neurons carry the sensory impulses from subcortical areas to cerebral cortex.

21. Spinal cord The dorsal horn of the spinal cord is the site where the primary afferent fibres synapse with second-order neurons. It is also where complex interactions occur between excitatory and inhibitory interneurons and where descending inhibitory tracts from higher centres exert their effect

22. The dorsal horn is divided into laminae (called Rexed laminae). Lamina II is also known as the substantia gelatinosa and this extends from the trigeminal nucleus in the medulla, to the filum terminale at the caudal end of the spinal cord. C fibres terminate in lamina II and Ad fibres terminate in laminae I and V. Ab fibres (light touch and vibration) enter the cord medial to the dorsal horn and pass without synapse to the dorsal columns. They give off collateral branches to the dorsal horn which terminate in several laminae ( IIIeV ). They also synapse directly with terminals of unmyelinated C fibres in lamina II. Laminae II and V are important areas for the modulation and localization of pain.

23. medulla Medulla has a region made up of both white and gray matter called reticular formation. It is the centre for various nuceli formation Reticular formation plays an important role in monitoring the impulses that travel the brain. It controls the overall activity of brain either by enhancing or inhibiting the impulses.

24. thalamus Thalamus acts as relay station for most of the communication between brain stem, cerebellum and cerebrum. As the impulses arrive at thalamus it makes assessment and direct the impulses to appropriate regions in higher centres for interpretation and response.

25. Cortex Brain areas for perception of pain: Sub cortical areas: hypothalamus, limbic system and thalamus Cortical areas: S1 and S2 in the somatosensory cortex. Insula and the anterior cingulate cortex

26. Neurotransmitters of pain they bathe the nociceptors, activating and sensitizing them. Prostaglandins and bradykinin sensitize nociceptors to activation by low-intensity stimuli. Histamine and 5-HT cause pain when directly applied to nerve endings. Hydrogen ions and 5-HT act directly on ion channels on the cell membrane, but most of the others bind to membrane receptors and activate second-messenger systems via G proteins.

27. Receptor potential It leads to development of local circuit which is later transmitted as action potential It doesn’t obey all or non phenomenon

28. Action potential

29. Neural Pain Pathways

30. Pain processing pathways It includes ascending and descending pathways In ascending pathways spino thalamic and spino reticular pathways play a major role in pain transmission to higher centres . Spino thalamic pathways includes neo spinothalamic and paleospino thalamic tracts

31. Ascending tracts

32. Neospinothalamic tract • Neurotransmitter - Glutamate • A∂ fibres transmit mechanical and thermal pain. • Termination in the spinal cord : Lamina I (Lamina Marginalis ) of the dorsal horn. • Excite second-order neurons

33. fast type A pain fibers   there excite second-order neurons, to long fibers that cross immediately to the opposite side of the cord through the anterior commissure and then turn upward, passing to the brain in the anterolateral columns. terminate reicular areas of the brain stem ventrobasal complex along with the dorsal column–medial lemniscal tract for tactile sensations. terminate in the posterior nuclear group of the thalamus, which transmit the signals to somatosensory cortex. terminate mainly in lamina marginalis of the dorsal horns

34. Capability of the Nervous System to Localize Fast Pain in the Body. The fast-sharp type of pain can be localized much more exactly in the different parts of the body than can slow-chronic pain. It is believed that glutamate is the neurotransmitter substance secreted in the spinal cord at the type A pain nerve fiber endings.  

35. Paleospinothalamic tract Type C fibres Neurotransmitter – Glutamate and Substance P Termination in spinal cord : Lamina II and Lamina III (Substantia Gelatinosa )

36. type C pain fibers, transmit some signals from type A fibers   peripheral fibers terminate in the spinal cord almost entirely in laminae II and III of the dorsal horns, which together are called the substantia gelatinosa. pass first through the anterior commissure to the opposite side of the cord, then upward to the brain in the anterolateral pathway. reticular nuclei of the medulla, pons, and mesencephalon;

37. Descending pain pATHWAY Analgesic pathway that interferes with pain transmission is often considered as descending pain pathway At synaptic level, analgesic fibers release neurotransmitters and inhibit the pain transmission before being relayed to brain. Neurotransmitters released by the fibers of analgesic pathway are serotonin and opiate receptor substances namely enkephalin, dynorphin and endorphin.

38. Facial pain pathway Facial pain is mainly mediated by trigeminal nerve

39. Special Capability of Pain Signals to Arouse Overall Brain Excitability. Electrical stimulation in the reticular areas of the brain stem and in the intralaminar nuclei of the thalamus, the areas where the slow-suffering type of pain terminates, has a strong arousal effect on nervous activity throughout the entire brain. In fact, these two areas constitute part of the brain’s principal “arousal system,”. This explains why it is almost impossible for a person to sleep when he or she is in severe pain.

40. Genes involved in pain

41. Applied aspects 1. Analgesia :Analgesia means loss of pain sensation. 2. Hyperalgesia :Hyperalgesia is defined as the increased sensitivity to pain sensation. 3. Paralgesia :Abnormal pain sensation is called paralgesia.

42. Assessment of pain Acute pain Chronic pain The Brief Pain Inventory (BPI) 0–10 NRS The BPI also asks the patient to rate how much pain interferes with seven aspects of life: general activity Walking normal work relations with other people Mood Sleep enjoyment of life. The BPI asks the patient to rate the relief they feel from the current pain treatment.

43. others McGill pain questionnaire Grade chronic pain severity scale Quantitative sensory testing

44. Sensory stimulation Analgesics pychological Medcinal therapy Electro acupuncture Neo epinephrine blockers Anti histaminics tranqulizers Anti microbials Analgesic balm Anti convulsant Anti inflamatory Anti deppresant nuerolytics Non narcotic narcotic adjuvant To arrest primary pain output Interruption in pain cycle Symapthetic blockage Trigger point therapy Dietary supplements cutaneuous Local anesthesia Transcutaneous percutaneou Trigger point therapy Deep heat therapy exercise Management of pain

45. References: Bell’s Orofacial pains Guyton textbook of medical physiology Sembhulingam physiology text book Burkets oral medicine Anil Ghom oral medicine A K JAIN textbook of physiology Moayedi M, Davis KD. Theories of pain: from specificity to gate control. J Neurophysiol 109: 5–12, 2013. The anatomy and physiology of pain by Charlotte E Steeds