Physio 2 - Neuro 1

drraythe's version from 2015-06-09 01:31

Neurophysiology, introduction and somatosensory system

Question Answer
what are the three basic functions of the nervous system?(1) detect stim. and transmit this info to CNS via sensory (afferent) neurons. (2) processing info and and decision making (interneurons or association neurons). (3) transmisson of response to decision to effectors (efferent/motor neurons)
4 sensory modalities of the somatosensory system are?Touch, proprioception, pain, and temperature
5 basic steps (movments) of a stimulation?transduction -> transmission -> modulation -> projection -> perception
sensory receptors are what order neuron?first order
what is transduction?when stimulating energy is transferred into electrical energy
what does decussate mean?cross over
ascending system composed of a 3-neuron chain...what are they?first order, second order, third order
first order neuron, aka sensory neuron. dendritic zone? cell bodies? terminate/synapse where?dendrites are the sensory receptors. cell bodies in dorsal root ganglia (unless cranial nerve, then in brain stem), terminate/synapse in dorsal grey horn with 2nd order neuron and/or LMNs for reflexes
second order neuron....cell bodies where? what do axons form--and where? decussate where? terminate/synapse where?bodies in dorsal grey horn. axons form ascending tracts in the white matter. decussate in spinal cord OR brain stem, terminate or synapse in thalamus or reticular formation (if synapse, w/ 3rd order neuron)
third order neuron...cell bodies where? axons project where?cell bodies in thalamus, etc. axons to somatosensory cortex
what is the somatosensory cortex responsible for?PERCEPTION (concious experience of the incoming stim.)
what is/ causes the cortical map?3rd order neurons end in DESIGNATED locations of corex...each area dedicated to a specific sense
what is rapid adaptation? receptors involved?sensory receptors adapt w/in secs or milisecs. PHASIC receptors. designed to register quick changes in stim strength. (rapidly set your gun to phase!)
what is slow adaptation? receptors involved?sensory receptors continue to transmit impulses as long as stim exists, frequency only decreases slightly. TONIC receptors. (keeps CNS appraised of body proprioception, baroreceptors, etc)
definition of pain? purpose?unpleasant sensory and emotional EXPERIENCE associated with actual or potential tissue damage. purpose is protection mechanism.
pain receptors are called? their description? where are they present? the transduction of pain is?nociceptors...have free nerve endings. present in all tissue except brain. nociception.
greatest to least amount of nociceptors in tissues?skin (somatic superficial pain) > muscles and joints (somatic deep pain) > organs (visceral pain)
two parts of pain process?generation of pain- first pain. maintenance of pain-second pain.
nerves associated with generation of pain? description of the fibers and the type of sensationA-delta fibers, myelinated. Sharp, immediate, stinging localized pain (first pain)
nerves associated with maintenance of pain? description of the fibers and the type of sensation, any additional factors?activated nociceptors release chemicals / excitatory neurotransmitters (SUBSTANCE P, CGRP[calcitonin-gene-related-peptide]) which cause more pain and stim release and production of inflammatory mediators. mediators activate nociceptors and maintain long lasting pain via C-fibers (unmyelinated) = second pain
what stims release of inflammatory mediators? what are the inflammatory mediators, where do they come from?substance P and calcitonin-gene-related-peptide(CGRP) stim release of inflammatory mediators. Mediators are released from tissue macrophages and WBCs. Include histamine, prostaglandins, bradykinin, cytokines.
how does inflammatory soup effect the transduction channels? (2)temporary changes....(1) channels widen for extended opening of channels (achieved via phosphorylation of channel proteins) and (2) insertion of new channels and receptors (via gene expression)
what does the inflammatory soup effecting the transduction channels accomplish?facilitate ionic flow and amplification of signal transmission (so nociceptors MORE SENSITIVE to stim.) -> this is to increase protection to the area
what are the two forms of sensitization? definitions?HYPERALGESIA (exaggerated pain response to noxious stimulus) and ALLODYNIA (pain response to non-noxious stim)
when does pain sensitization typically occur?as the injury is healing
basic tract of ascending pain pathway?A+C fibers enter SC via dorsal root -> dorsal horn -> synapse with 2nd order and use excitatory neurotransmitters (substance P, glutamate) -> neurons enter SPINOTHALAMC TRACT(STT) in LATERAL FUNNICULUS (contra in primates, ipsi and contra in animals). -> STT then projects to thalamus for A fibers (aka neo-STT) //or// reticular formation/limbic system for C-fibers aka paleo-STT -> then somatosensory cortex
what does the paleo-STT (spinothalamic tract) do other than just the C-fiber stuff?autonomic responses (pulse, blood pressure, sweat), emotional and B/h responses (fear, avoidance), and maintains arousal and wakefullness
what paths are responsible for modulation/inhibition of paindescending analgesia pathways
where do analgesia pathways originate? where do they descend?originates in cortex, thalamus, and brain stem. descend in lateral funiculus.
where do analgesia pathways synapse? where do they end?synapse with ascending pain neurons and end on inhibitory interneurons in the dorsal horns.
where do the inhibitory interneurons synpase? what are the inhibitory interneurons' inhibitory neurotransmitters?DFDFSGDSG


Question Answer
where is the pain signal blocked in inhibition of pain? what are the neurotransmitters used?blocked where 1 synapses to 2nd order. inhibitory NTs are endogenous opioids (enkephalins, endorphins, and dynorphins, GABA, glycine
where are endorphins released aside from in analgesia pathways?hypothalamus
explain chronic pain. charaterized by?no physiological purpose and persists in absence of tissue injury. charaterized by hypersensitivity of pain transmission system
what are the two mechanisms of chronic pain? (neuroplasticity)1) peripheral sensitization (nociceptor remodeling from inflammatory mediators) 2) central sensitization (hypersensitivty upon strong stimulation, like in surgical incisions)
what is the key to preventing chronic pain?preemptive analgesia
what type of animal would show less obvious signs of pain?prey animals
how to test for superficial pain? deep pain?superficial= skin prick. deep = pinching digits and joints
why must multimodal analgesia be used?because of different NT patterns and different pain pathways with variety of excitatory and inhibitory NTs
what do proprioceptive receptors constant monitor, and how?muscle length+tension via muscle spindles, tendon length+tension via tendon organs, joint angulation+rotation via joint receptors
what are muscle spindles?groups of 3-10 specalized muscle fibers (INTRAFUSAL) in a capsule parallel to ordinary muscle fibers (extrafusal)
how do muscle fibers work?polar ends of intrafusal fibers can contract (innervated by gamma motor neurons) the midpiece acts as the sensory receptor (monitors changes in length, initiates stretch reflexes, maintains and adjusts muscle tone)
what is a tendon (golgi) organ composed of? how is it innervated?collagen fibers in a capsule...sensory fibers (Ib) form dense network of dendrites around fibers.
what does a tendon organ monitor? how?monitors muscle tension by being situated at muscle-tendon junction in series with muscle fibers so the organ stretches as muscle contracts
joint (kinesthetic) receptors are located where? what are they? responds to what?within and around joint capsules. are free nerve endings, ruffini/pacinian corpuscles. respond to changes in PRESSURE and MOVEMENT

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