Neuroscience Part 2 Lecture 7 PDF

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Neuroscience Lecture Notes
Part 2 Spring Term
Lecture by Tim Salomons...

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Neuroscience Lecture 7- Pain 1 What is Pain?  an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage (IASP, 1994) Dimensions of Pain  Melzack and Casey (1968) highlighted three dimensions of pain: 1. Sensory-discriminative: information about the intensity, location, quality and temporal and spatial aspects of pain 2. Motivational-affective: the emotional component; determines avoidance behaviours 3. Cognitive-evaluative: Evaluation of the meaning of the pain and the context in which it occurs Bottom Up View to Pain  Pain determined by properties of the stimulus and the type of receptor that encodes it  Descartes (1664): stimulus activates a fiber that sends a message to the brain, like a cord ringing a bell  Specificity theories posit dedicated fibers, dedicated pain pathways and dedicated brain regions  Late 19th century discovery of specific touch receptors for specific qualia  Pacinian corpuscles: rough surfaces and vibration  Meissner’s corpuscles: light touch and speed of stimuli  Merkel’s discs: gentle localized pressure  Ruffini’s corpuscles: vibration and stretching of skin and tendons Specific Pain Receptors  There are receptors that appear to be specific to the experience of pain, or at least to specialize in levels of stimulation that would ordinarily cause pain  Nociceptor (Charles Sherrington (1906) and Perl and colleagues (1960s)  A nerve ending that responds to noxious stimuli that could produce tissue damage.  Not a pain receptor as not always activated through pain  Two types of nociceptors 1. A-delta fibers Thick, myelinated, fast conducting neurons Mediate the feeling of initial fast, sharp, highly localized pain 2. C fibers Very thin, unmyelinated, slow-conducting Mediate slow, dull, more diffuse, often burning pain Higher Order Pain Pathways  From the spinal cord to the brain  Spinothalamic Tract:  2nd order tracts from dorsal horn decussate just above spinal level  Ascend to contralateral thalamus (medial dorsal, VPL)

3rd order neurons ascend to somatosensory cortex and other sensory regions Largely responsible for coding sensory aspects of pain (e.g. location) as well as mediating fast motor responses  Spinoreticular Tract:  2nd order tracts decussate and reach reticular formation in brainstem  Project to intralaminar nuclei of thalamus, hypothalamus and cortex  Involved in emotional aspects of pain  

Challenges to the Bottom Up View  Peripheral input cannot account for the variety of pain experienced e.g. cognitive or emotional pain  Cognitive modulation of pain  Distraction  Placebo  Perceived control  Variable link between pain and injury  Congenital analgesia- People do not sense physical pain coming in from outside stimuli. E.g. soliders breaking ankles on the battlefield but not feeling pain until in infirmary  Episodic analgesia (Beecher et al, 1959)- Episodic absence of pain in response to a normally painful stimulus. This was characterised in 6 states by Melzack and Wall (1988): 1. The condition has no relationship to the severity or the location of the injury. 2. No simple relationship to circumstances - occurs in battle or at home. 3. Victim fully aware of injury but feels no pain 4. Analgesia is instantaneous 5. Analgesia lasts for a limited time 6. Analgesia is localised, pain can be felt in other parts of the body  Phantom Limb Pain (Staehelin, 1999)- appears to come from where an amputated limb used to be – is often excruciating and almost impossible to treat. Gate Control Theory (Melzack and Wall, 1965)  “Gate” in dorsal horn of spinal cord will allow ascending nociceptive signals through to the brain  Opened or closed on basis of which fibers are activated: gate can be open if nociceptive fibers are active and closed if non-nociceptive fibers are active  Gate can be closed by descending signals from brain Descending Controls  Periacqueductal Gray (PAG)  Receives ascending nociceptive input from the dorsal horn and afferent input from hypothalamus and amygdala (Bandler and Keay, 1996)  Rich in opioid receptors  Also involved in defensive and fear responses.  Rostral Ventromedial Medulla (RVM)  Particularly strongly connected with the PAG (Beitz, 1982)

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Receives minimal input from spinal cord and projects heavily to the spinal cord dorsal horn Involved in sensitizing the periphery to sensory input (central sensitization) (Urban and Gebhart, 1999) Thought to contain both “on” and “off” cells (Fields and Basbaum, 1999)

Behavioural Activation of Descending Modulation  Stress-induced analgesia is blocked by RVM lesions and naloxone (Watkins & Mayer, 1982)  Conditioned fear induced analgesia blocked by lesions of amygdala, RVM or naloxone injected in PAG (Watkins, 1982)  Safety signals block opiate analgesia  Shock given followed by a light, the light will become the safety signal  Lesions of RVM block this effect (Wiertelak, 1992)  PAG associated with modulation of pain  Distraction (Tracey, 2002)  Perceived control (Salomons, 2007)  Competing nociceptive input (Sprenger, 2011)...