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CHAPTER 11 The Body Senses and Movement The Body Senses Movement
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Information about our body is processed by 2 main systems: – somatosensory system –vestibular system. Somatosenses include – Proprioception : Concerned with movement and spatial orientation – Skin senses : tell us about conditions at the surface of our body, – Interoceptive system: concerned with sensations in our internal organs. Vestibular system informs the brain about –Body position –Body movement.
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Proprioception –Sense that informs us about the position and movement of our limbs and body. –Often in the context of movement and spatial relations (where your butt is in relation to the seat of the chair) Skin senses include: –Touch: light touch to heavy pressure –Warmth to cold –Pain. The skin Senses
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Free nerve endings: –Simple processes at the ends of neurons. –Detect warmth, cold, and pain. Encapsulated receptors: –Form all other receptors –More complex structures enclosed in a membrane. –Their role is to detect touch. Two general types of skin receptors
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Cutaneous mechanoreceptors –respond to mechanical pressure or distortion caused by physical interaction, including pressure and vibration –Cutaneous = in the skin There are several kinds of these receptors embedded in our skin: – Ruffini's end organ : detect sustained pressure – Meissner's corpuscle : detect changes in texture, slow vibrations – Pacinian corpuscle: deep pressure, fast vibrations – Merkel's disc: detect sustained touch and pressure skin receptors for detecting touch and pressure
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Vestibular sense : –helps maintain balance –provides information about head position and movement. Vestibular organs in the inner ear –semicircular canals –the utricle, –the saccule. Parieto-insular-vestibular cortex : –Vestibular system sends projections from the cerebellum and the brain stem to the insular cortex of the temporal lobe –Provides information regarding position of body in space and movement The vestibular Senses
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Somatosensory Pathway First neuron junction : –Cell body on dorsal root ganglion of the spinal nerve or cranial nerves –Forms initial connection between body and spinal cord Second neuron junction : –Cell body either in the spinal cord or in the brainstem. –Second neuron's ascending axons will cross (decussate) to the opposite side either in the spinal cord or in the brainstem. –The axons of these neurons terminate in the thalamus or reticular system or cerebellum. Third Neuron junction : –Exists for touch and some types of pain: –Cell body in the VPN of the thalamus –Ends in the postcentral gyrus of the parietal lobe
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Pathway into brain Somatosensory cortex –From thalamus, body sense neurons go to their projection area: –located in the parietal lobes –just behind the primary motor cortex and the central sulcus. Most of the neurons cross from one side of the body to the other side of the brain – Contralateral (crossing) vs ipsilateral (not crossing) –Touch of an object held in the right hand registered mostly in left hemisphere. –Why do you think this is?
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Dermatomes : –Body is divided into segments –Each segment served by a spinal nerve. –We process information from each dermatome –Damage to a particular spinal nerve results in damage to the corresponding dermatome Divided into several subdivisions: – Cervical : head, upper neck – Thoracic : lower neck to chest – Lumbar : middle – Sacral or coccygeal: tail The Body Senses
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The labels identify the nerve. – Letters = part of the spinal cord where the nerve located – Numbers = nerve ’ s position within that section. For example: Areas I, II,and III on the face innervated by branches of the trigeminal (fifth) cranial nerve. Amount of brain devoted to each area depends on how much we use/sense from that body area Remember the homunculus The Body Senses
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Somatosensory cortices Primary somatosensory cortex –Consists of four areas –Each contains a map of the body –Each plays a role in processing sensory information for the body. Secondary somatosensory cortex –Receives input from the left and the right primary somatosensory cortices, – Combines information from both sides of the body. –Neurons in this area particularly responsive to stimuli that have acquired meaning (e.g., association with reward). –Connects to the part of the temporal lobe that includes the hippocampus Hippocampus critical for learning, May determine whether a stimulus is committed to memory.
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The primary somatosensory cortex also projects to the posterior parietal cortex Posterior parietal cortex: –Association area –Brings together the body senses: somatosensory, vision, and audition. –Determines body’s orientation in space, the location of the limbs, the location in space of objects detected by touch, sight, and sound. –It integrates the body with the world. Posterior parietal cortex
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Synesthesia: –the experience of some kind of cross-activation from one sense to another –the condition of being prone to such experiences. Several causes: –Brain damage –Psychodelic drug activation –Developmental synesthesia Why? –Activation of one cortical area by an inducing stimulus (say, letters) causes co-activation of another cortical area (say, the color area), –This produces additional color perceptions or associations. –Letters thus come in specific colors Synesthesia: too much integration of sensory areas
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Pain processing: – begins when free nerve endings stimulated by intense pressure temperature damage to tissue. There are three types of pain receptors. –Thermal pain receptors: respond to extreme heat/cold. –Mechanical pain receptors: respond to intense stimulation like pinching/cutting. –Polymodal pain receptors: activated by both thermal and mechanical stimuli chemicals released when tissue is injured. Pain
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Endorphins function both as: –Neurotransmitters –Hormones –Act at opiate receptors in many parts of the nervous system. Pain = one of stimuli that release endorphins –Endorphins released under certain conditions. Physical stress Pain Long term exertion endorphins
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Ronald Melzack and Patrick Wall In the spinal cord: Pain neurons release: –Glutamate – Substance P : neuropeptide involved in pain signaling. released only during intense pain stimulation. Gate theory states that there are two kinds of pain fibers: –some specific nerve fibers transmit pain to the spinal cord –input of other nerve fibers inhibits the transmission of pain. Gate Theory
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Both groups of pain fibers meet at a sort of ‘mediator' in the spinal cord called the substancia gelatinosa. Gate theory : Proposes a balance between stimulation of the pain fibers and inhibition of that stimulus, –pain is perceived only if the pain input overrides the inhibition of pain –Is the sum of the signals transmitting pain + signals transmitting inhibiting of pain –Thus pain is “gated” : if more pain sensation than not pain sensation from free receptors, then perceive sensation as pain Gate Theory
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Periaqueductal gray area: PAG –Brain stem structure –Contains large number of endorphin synapses. –Stimuli like pain and stress cause the release of endorphins in the PAG –Endorphin release inhibits the release of Substance P, closing the pain “gate” in the spinal cord. Activation of the endorphin circuit has multiple neural origins, for example: –Cingulate cortex during placebo analgesia –Amygdala in the case of fear-induced analgesia. –Response to pain signals –Response to chronic stress signals Brain response to pain
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Cannabinoid receptors respond to the active ingredient in marijuana In rats: blocking cannabinoid receptors in the periaqueductal gray reduces analgesia produced by brief foot shock. This suggests that cannabinoids also –Are internal pain relievers – share the neural gating system used by endorphins –may explain ‘pleasure’ sensation Cannabinoid substances may be useful as analgesics Cannabinoid receptors
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Phantom pain: –Pain that is experienced as being located in the missing (amputated) limb. –70% of amputees experience –Phantom pain IS a real sensation : brain not know that limb is missing –Significant problem in post-amputation pain management. Phantom pain
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The phantom “pain” originates in the brain. –Neural circuits for movement involve many movement areas After amputation: missing limb still has neural contribution to a movement When move your body, those circuits are stimulated –Brain is interpreting the state of the “missing” limb via the stimulation of those old remaining circuits Awareness of the details of limb's shape/perceived ability to move it tend to fade with time. –Over time, old neural connections fade (no longer stimulated because the limb associated with them is gone) –New circuits form that do not include the neural stimulation caused by the missing limb Most amputees report continuing to feel some phantom sensations throughout the remainder of their lives. Phantom pain
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Neural mechanisms which permit perception of phantom limbs are well recognized: –Major muscles in residual limb tense up several seconds before cramping phantom limb pain begins Remember: those muscles associated with movement in missing limb Brain interprets this as if the missing limb itself was cramping Muscles remain tense for much of duration of episode. –Muscle fatigue sets in –Reduced blood supply –Eventually, pain sensation in remaining muscles –But, because circuits are tied to missing limb, feel as if missing limb is painful ! Burning phantom limb pain closely associated with reduced blood flow in residual limb- is a sensation of a lack of circulation –Brain acting like limb still there: interprets residual limb activity as if it was activity in the missing limb –Assumes that if residual muscle is “hurting”, the missing limb must be too! Phantom pain
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What is brain doing? Investigated brain activity for missing arm –Researchers noted that stimulating the amputee’s face often produces sensations in phantom (missing) arm –Team of researchers in Germany used brain imaging to map face and hand somatosensory areas in upper-limb amputees. In phantom limb pain patients: –Neurons from the face area appear to invade the area that normally receives input from the missing hand. –Thus, as face moves, brain processes this as movement of limb, and pain reaction to movement –As if neurons for one area of the body spread and take over the neurons for the missing limb…except the body doesn’t know it ISN’T the missing limb Phantom pain
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Main treatment is NOT pain meds, but fixing the miscommunication in the brain through BIOFEEDBACK Why is biofeedback helpful? –Teach the amputee’s brain to recognize that limb is missing –The specific aim of the treatment: teach amputees with phantom pain to habitually and unconsciously keep their residual limbs as warm and as relaxed as the intact limb. Teach them to increase muscle temperature Teach them to reduce cramping and muscle tension in surrounding area –Disconnect neural patterns involving the missing limb! Phantom pain: Treatment
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Have to explicitly TEACH the relationship between sensation and the missing limb: –Feel the muscle tension/temp changes in the tissue surrounding the missing limb –Relate those sensations to the pain sensations “in the missing limb” Muscle tension and temperature awareness training –Often use mirrors or biosensors: –Show muscle tension in surrounding muscle areas –Have amputee identify pain sensation that goes with the tensing of surrounding muscles: SEE the tension and FEEL the pain –Have them learn to relax surrounding muscles and feel lessening of pain SEE the relaxation and FEEL the lessening of pain Begin to learn to control these parameters…..lots and lots of trials and practice Phantom pain: Treatment
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After several weeks, patients begin doing the exercise at home and in their normal work environment: –Want the relaxation to occur with the onset of pain –Want to make it a habit: When feel pain in missing limb-engage in relaxation, pain goes away! –Soon the body does it automatically, as a habit Generalize awareness of changes in the parameters to their normal environment. –Almost automatically relax when feel the phantom pain –Practice the technique everywhere! The more you practice generalization, the less pain you will feel! Phantom pain: Treatment
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