Neurobiology- Polston Flashcards
Pain and pain management is a big part of what you will deal with.
In terms of drug prescribing chronic pain management is all about SLOW pain stuff
Mirror therapy
-one of the therapies used to deal with phantom limb pain
What is pain?
a sensory experience -a series of neurochemical events or responses specifically response to noxious damaging or threatening stimuli occurs when nociceptive pathways from sensory receptors to the brain are stimulated -function of pain is a primitive lower level defensive response that is supposed to keep you alive; when you get to places that may damage your system, we turn on our pain system to take us away from the damaging event; it is an adaptive response -like other somatosensory response pain is a perceptual experience and unpleasant experience that is associated with negative emotions and responses to either actual or potential tissue damage. -pain is all in the head (you don’t feel the pain if it doesn’t get to the brain)
What is pain and nociception? Pain and nociception are separable events. Under normal circumstances they go together.
Pain is your sensory perception of the pain. Nociception is the actual damaging event that will trigger neurochemical events. paraplegia with no perceptional awarements to sensory to your leg; someone has broken your leg with a hammer; no pain because the perception does not reach your brain nerves that convey pain to your brain are firing even though there is nothing wrong with your leg; its something wrong with your pathway; pain in the absence of nociception you could have nociception in the absence of pain if the signal doesn’t make it to your brain to be perceived OR you could have pain without nociceptors that have signal coming in for no good reason
What are the two main categories of pain? What’s the difference between the two?
FAST PAIN -happens at the time of the insult (immediate component) -very acute, very sharp -actual pain from the damage being inflicted -happens faster for a number of reason: type of axons that conveys fast pain (Adelta which are lightly myelinated) -the first synapse in the pain pathway is in the dorsal horn of the SC the primary sensory afferent synapse in the peripheral???????(11)that synapse uses glutamate (NMDA channel receptors= ionotropic receptors) as the NT -time of stimulus to get from periphery to brain is relatively fast -easy to localize (you know precisely where the pain is occuring) -typically peripheral pain (at the skin or muscle at the periphery) SLOW PAIN -pain after the event -about protecting the injured area so you don’t hurt it again -C-fibers= unmyelinated (slower to get to the brain) -form the -C-fibers and unmyelinated -the gift that keeps on giving -not well localized (the whole hand is throbbing) -occurs in the periphery and mostly deep pain (stomach pain) -first synapse in the same region as fast which is the dorsal horn but not uses Substance P neurons; these are neuropeptide which are very slow to make that work through metabotropic receptors
SKIN MECHANORECEPTORS
-we’re talking about pain and temperature which use the same pathway and free nerve endings (Always together) -they can be superficial in layers of the skin -they can contain Nociceptor and Thermoreceptors and wrap around Hair follicles
NOCICEPTORS
Free nerve endings: -Widespread in superficial layers of the skin, periosteum/cranium, arterial walls, joints -Sparse innervation of most deep tissues -No innervation of central neural tissue (in the SC and brain themselves); has interesting connotations (skull, meninges, muscles); why you can anesthetize the pt and cut open their skull with pt awake it heightens their sensitivity which lowers the threshold for the primary afferent neuron; free nerve endings have a higher threshold for stimulus you would want a higher threshold for pain conveying than fine touch coneying; it makes sense that pain pathways are high threshold pathway (touching clothes would hurt if the pain neurons were low threshold) Receptor properties vary -Adequate stimulus depends on modality (crushing, cutting, etc.) -Receptive field size varies between different pain modalities. 100 mm for mechanical (sharp have small receptive field because we know exactly where that stimulus is as opposed to burning pain that has large receptive fields) -Little to no sensory adaptation (in regards to pain conveying neurons) -these are TONIC firing neurons (no adaptation) The perception of pain is your driving force the escape these damaging events.
Many stimuli that can cause pain.
Responsive to multiple stimuli Mechanical stimuli -lack of specialized endings raises threshold (breeches the membrane integrity of the free nerve endings) -may be somatic (in muscle) or visceral (Cramps) Chemical stimuli -exogenous and endogenous algesic factors (HCl chemical or even HCl in the stomach) -may be somatic or visceral Thermal stimuli -heat : > 43ºC (113ºF) -cold: < 15ºC (59ºF) -usually somatic (we are thermoregulators and have a distinct region of temp our body will experience) this is all about damage; if it’s going to hurt you then there will be pain Itch and Tickle -associated with nociceptors (cross talk with itching and pain as with mosquito bite and you put ice on it or put your fingernail in the bite) -travel in spinothalamic pathway
THERMAL RECEPTORS
-More cold receptors (cool spots) than warmth receptors. -Warmth transmitted by C and Ad fibers -Noxious heat transmitted by Ad fibers (finger in the candle) -Cool transmitted mainly by Ad fibers the more noxious the stimulus the faster you need to know about it -Slow and incomplete sensory adaptation; we do have adaption to slow cold and hot temp -Conveyed through anterolateral (spinothalamic) system
PATHWAYS FOR PAIN AND TEMPERATURE: Pain and temperature sensation from BODY
Pain and temperature from the body First order neurons synapse on second order neurons in the ipsilateral dorsal horn (Laminae I and II), IPSILATERAL SECOND order neurons CROSS THE MIDLINE (in the anterior commissure) and ascend contralaterally in the spinothalamic tract, to synapse on neurons in the VPL nucleus of the thalamus. (some collateral fiber go to VPI for affective aspects, suffering which is not a strict thalamic nucleus that causes feeling of suffering for slow pain–CHRONIC PAIN) Third order neurons project from the thalamus to the primary sensory cortex. CONTRALATERAL
Primary order neurons of pain, temperature, touch, proprioception
ALL located in DRG
PATHWAYS FOR PAIN AND TEMPERATURE: Pain and temperature sensation from the FACE
First order neurons from the trigeminal ganglion descend to synapse onto second order neurons in the ipsilateral spinal trigeminal nucleus. Second order neurons cross the midline and ascend contralaterally in the spinal lemniscus (at the level of the cervical spinal cord) to synapse on third order neurons in the VPM nucleus of the thalamus (VPI for affective aspects) may experience a toothache when you have suffered damage to the cervical ganglion (remember nociception and pain can be separated) Third order neurons project from the thalamus to the primary sensory cortex. (is DIFFERENT for fast and slow pain)
BROWN-SEQUARD SYNDROME
what is brown-sequard syndrome? Brown-Sequard syndrome (BSS) is a rare neurological condition characterized by a lesion in the spinal cord which results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side. -for pain and temperature, second order neurons cross over the midline Ipsilateral signs Loss of fine touch, vibration, proprioception Contralateral signs Loss of pain and temperature, crude touch
PATHWAYS FOR PAIN AND TEMPERATURE LISSAUER’S TRACT
-first order neuron comes in and synapses in nucleus cuneatus and nucleus fasciculus -each dermatome associated with one spinal nerve and in the fine touch pathway that is the only place that sensation is coming in from; so a lesion that hits that level will knock out fine touch sensation -pain pathway is different in that the first order neuron comes in and looks for second order neurons in the ipsilateral SC up or down 1-2 SC levels; however if you have lesion at T2 you may not lose all your pain sensation because they descend or ascend 1-2 levels Pain and temperature sensation Lissauer’s tract Axons from some first order neurons conveying pain and temperature synapse immediately onto second order neurons, but many ascend or descend 1-2 levels in Lissauer’s tract before synapsing Some pain and temperature sensation is therefore spared when a spinal hemisection is discrete. Sensory sparing reflects branching of afferent pain fibers (Lissauer’s tract) Lissauer’s tract is is a stack of input NOT a longitudinal input like dorsal column tract; allows you to receive inputs even if there is damage in the dorsal horn; if you damage the spinal nerve none of those branches will work but if they damage in the dorsal horn you have little branches that may come in above it and allow you to detect pain and temp from that dermatome blue is fine touch green is pain and temperature
PATHWAYS FOR PAIN AND TEMPERATURESPINOTHALAMIC TRACT FAST PAIN
fast pain is a newer system Fast Pain – Neospinothalamic tract Neospinothalamic tract contains mainly Ad fibers that contain fast pain. Fibers are primarily from the most dorsal parts of the SC which Rexed’s laminae I and II (marginal zone and substantia gelatinosa) Sparse projections (on the way up to the thalamus) to the reticular formation (arousal); to get away from that damaging stimuli real quick!!! Major projection to VPL of the thalamus Cortical projections for location and quality of stimulus you are getting sensory projections to thalamus to the cortex real quick (no branching really cuz again you gotta go real quick); does not sightsee lol
PATHWAYS FOR PAIN AND TEMPERATURESPINOTHALAMIC TRACT SLOW PAIN
slow pain is an older system Slow Pain – Paleospinothalamic tract Evolutionarily older pathway Paleospinothalamic tract contains mainly C fibers that convey slow pain (especially visceral). Second order neurons are primarily from Rexed’s laminae II and III . Some synapse on interneurons in lamina V. Ascending tract projects widely to the reticular formation, periaqueductal gray, and limbic system Projections to VPL and intralaminar thalamus nucleus (which is the suffering nucleus) Limited role for somatosensory cortex; does a lot of sightseeing!!!; you are NOT going straight to the thalamus or straight to the cortex; relative particular information about where pain is coming from is useless to you! amygdala (learning center will get some fibers)
PATHWAYS FOR PAIN vs. FINE TOUCH COLLATERAL BRANCHING
This reemphasizes the places we would see branches to in a slow pain pathway but not a fast pain pathway and definitely not a fine touch as fine touch is all about the cortex!
Where are we perceiving the slow pain?
mainly in the thalamus Collateral branching in the paleospino- thalamic tract allows subcortical responses -Arousal centers in the reticular formation -Emotional responses from the limbic system -Subcortical pain perception - Thalamus Evidence for subcortical pain perception -Removal of somatic sensory cortex does not prevent slow pain perception (cortex is about quality of pain; thalamus is about perception of the pain??) -Stimulation of somatosensory cortex induces mild pain only -Cortical awareness relates mostly to perception of the quality of pain -Thalamic pain syndrome
Deep pain is about slow pain systems.
Slow pain – conveyed mainly by C fibers. Few Ad fibers in deep structures Poorly localized (when you break your arm you don’t feel the pain mapped out to that specific site) Frequently associated autonomic responses such as with nausea, sweating, changes in blood pressure Often induces reflex muscle contraction. (but you really want to relax!) Extended muscle contraction exacerbates deep pain
VISCERAL PAIN is associated with internal organs and is SLOW pain.
Usually doesn’t convey small discrete stimuli. Requires diffuse stimulation of nociceptors throughout Due to either mechanical or chemical stimuli (not thermal) Variety of etiological factors -Ischemia: formation of acids, bradykinins, proteolytic enzymes. -Chemical stimuli: gastric juices -Smooth muscle spasm of hollow viscus (cramps and ischemia) -Overdistention of a hollow viscus (stretch and ischemia Most visceral pain comes from cramping or overextension of a hollow tube. C-fibers are fairly sparse innervated which means that if someone was to hit me with a needle it would hurt as it went through your deep tissues but it would be very unlikely to hit a pain fiber as the needle gets to your stomach. Most things that cause visceral pain are WHOLE organ events, you don’t need detailed innervation.
