The Sensory system Specific sensation depends upon brain region being stimulated. Receptor or nerve ending is stimulated. Sensory neuron transmits signal. Brain interprets signal. Sensory adaptation – Sensory receptors send signal at decreasing rate due to continuous stimulation.
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The Sensory system
Specific sensation depends upon brain region being stimulated.
Receptor or nerve ending is stimulated. Sensory neuron transmits signal. Brain interprets signal. Sensory adaptation
– Sensory receptors send signal at decreasing rate due to continuous stimulation.
From Sensation to Perception
Survival depends upon sensation and perception
Sensation is the awareness of changes in the internal and external environment
Perception is the conscious interpretation of those stimuli
Organization of the Somatosensory System
Input comes from exteroceptors, proprioceptors, and interoceptors
The three main levels of neural integration in the somatosensory system are:– Receptor level – the sensor receptors– Circuit level – ascending pathways– Perceptual level – neuronal circuits in the cerebral
cortex
Processing at the Receptor Lever
The receptor must have specificity for the stimulus energy
The receptor’s receptive field must be stimulated
Stimulus energy must be converted into a graded potential
A generator potential in the associated sensory neuron must reach threshold
Adaptation of Sensory Receptors
Adaptation occurs when sensory receptors are subjected to an unchanging stimulus– Receptor membranes become less responsive– Receptor potentials decline in frequency or stop
Adaptation of Sensory Receptors
Receptors responding to pressure, touch, and smell adapt quickly
Receptors responding slowly include Merkel’s discs, Ruffini’s corpuscles, and interoceptors that respond to chemical levels in the blood
Pain receptors and proprioceptors do not exhibit adaptation
Processing at the Circuit Level
Chains of three neurons (first-, second-, and third-order) conduct sensory impulses upward to the brain
First-order neurons – soma reside in dorsal root or cranial ganglia, and conduct impulses from the skin to the spinal cord or brain stem
Second-order neurons – soma reside in the dorsal horn of the spinal cord or medullary nuclei and transmit impulses to the thalamus or cerebellum
Third-order neurons – located in the thalamus and conduct impulses to the somatosensory cortex of the cerebrum
Receptive Fields
Area of skin whose stimulation results in changes in the firing rate of the neuron.
– Area of each receptor field varies inversely with the density of receptors in the region.
Back and legs have few sensory endings.– Receptive field is large.
Fingertips have large # of cutaneous receptors.– Receptive field is small.
Two-Point Touch Threshold
Minimum distance at which 2 points of touch can be perceived as separate.
– Measures of distance between receptive fields.
Indication of tactile acuity.– If distance between 2
points is less than minimum distance, only 1 point will be felt.
Lateral Inhibition
Sharpening of sensation.– When a blunt object
touches the skin, sensory neurons in the center areas are stimulated more than neighboring fields.
– No clear, sharp boundary. Will be perceived as a
single touch with well defined borders.
– Occurs within CNS.
Figure 10-6
Sensory Areas
Cortical areas involved in conscious awareness of sensation
Distinct area for each of the major senses
Sensory Areas – Primary Somatosensory Cortex
Located along the postcentral gyrus
Involved with conscious awareness of general somatic senses
Sensory Areas – Primary Somatosensory Cortex
Projection is contralateral – Cerebral hemispheres
Receive sensory input from the opposite side of the body
Sensory homunculus – a body map of the sensory cortex
Sensory Areas – Sensory Homunculus
Sensory Areas – Somatosensory Association Area
Lies posterior to the primary somatosensory cortex
Integrates different sensory inputs– Touch, pressure, and others
Draws upon stored memories of past sensory experiences
White MatterWhite Matter Anterior Funiculus (Anterior White Column)Anterior Funiculus (Anterior White Column)
Posterior Funiculus (Posterior White Column)Posterior Funiculus (Posterior White Column) Fasciculus Gracilis & Fasciculus CuneatusFasciculus Gracilis & Fasciculus Cuneatus
Lateral Funiculus (Lateral White Column)Lateral Funiculus (Lateral White Column)
Lamina IX ---------- Lamina IX ---------- Anterior Horn (Motor) CellAnterior Horn (Motor) Cell
Lamina X ----------- Gray CommissureLamina X ----------- Gray Commissure
Lamina of RexedLamina of RexedLamina of RexedLamina of Rexed
Spinal Nerves
A series of connective tissue layer surrounds each spinal nerve.
Epineurium-outermost layer, consists of a dense network of collagen fibers.
Perineurium-extend inward from the epineurium, dividing the nerve into a series of compartments.
Endoneurium-delicate connective tissue fibers.
Ventral and Dorsal Roots
In the vicinity of the cord, each spinal nerve divides into a ventral (anterior, motor) root and a dorsal (posterior, sensory) root.
Ventral roots contain mostly efferent nerve fibers and convey motor information.
Dorsal roots contain afferent nerve fibers and convey sensory information.
The axons of motor neurons whose cell bodies are located within the CNS in the ant. Horn emerge from the spinal cord to form ventral roots (motor).
Groups of sensory neurons , whose axons make up the dorsal roots lie outside the cord in the dorsal root ganglia or spinal ganglia of the PNS.
Peripheral distribution of Spinal Nerves
A typical spinal nerve has a white ramus(this contains myelinated axons), and a gray ramus (unmyelinated fibers that innervate glands and smooth muscles in the body wall or limbs)
A dorsal ramus(providing sensory and motor innervation to the skin and muscles of the back), and a ventral ramus (supplying the ventrolateral body surface, structures in the body wall and the limbs).
Each pair of nerves monitors a region of the body surface called a dermatome.
Nerve Plexuses
A complex, interwoven network of nerves is a nerve plexus.
The three large plexuses are the cervical plexus, the brachial plexus and the lumbosacral plexus. The latter can be further divided into the lumbar plexus and the sacral plexus.
White Matter of the Spinal Cord
Sensory and Motor Pathways
Most motor pathways:– Decussate at some point along their course– Consist of a chain of two or three neurons– Exhibit somatotopy
Tracts arranged according to the body region they supply
All pathways are paired– One of each on each side of the body
Fasciculus cuneatus and Fasciculus gracilis
Figure 12.33a
Posterior White Column-Medial Lemniscal PathwayPosterior White Column-Medial Lemniscal Pathway
(Tract of gall and burdach)(Tract of gall and burdach) Modality: Modality: Discriminative Touch Sensation (include Vibration) and Discriminative Touch Sensation (include Vibration) and Conscious Proprioception (Position Sensation, Kinesthesia)Conscious Proprioception (Position Sensation, Kinesthesia)
Receptor: Most receptors except free nerve endingsReceptor: Most receptors except free nerve endings
Ist Neuron: Ist Neuron: Dorsal Root Ganglion (Spinal Ganglion)Dorsal Root Ganglion (Spinal Ganglion)
Posterior Root - Posterior White ColumnPosterior Root - Posterior White Column
2nd Neuron: 2nd Neuron: Dorsal Column NucleiDorsal Column Nuclei (Nucleus Gracilis and Cuneatus)(Nucleus Gracilis and Cuneatus)
Termination: Termination: Primary Somesthetic Area (S I)Primary Somesthetic Area (S I)
Posterior White Column-Medial Lemniscal PathwayPosterior White Column-Medial Lemniscal Pathway
(Tract of gall and burdach)(Tract of gall and burdach) Modality: Modality: Discriminative Touch Sensation (include Vibration) and Discriminative Touch Sensation (include Vibration) and Conscious Proprioception (Position Sensation, Kinesthesia)Conscious Proprioception (Position Sensation, Kinesthesia)
Receptor: Most receptors except free nerve endingsReceptor: Most receptors except free nerve endings
Ist Neuron: Ist Neuron: Dorsal Root Ganglion (Spinal Ganglion)Dorsal Root Ganglion (Spinal Ganglion)
Posterior Root - Posterior White ColumnPosterior Root - Posterior White Column
2nd Neuron: 2nd Neuron: Dorsal Column NucleiDorsal Column Nuclei (Nucleus Gracilis and Cuneatus)(Nucleus Gracilis and Cuneatus)
Algogenic substances – chemicals released at the site of the injury
Nociceptors – afferent neurons that carry pain messages
Referred pain – pain that is perceived as if it were coming from somewhere else in the body
Peripheral Nerve Fibers Involved in Pain Perception
A-delta fibers – small, myelinated fibers that transmit sharp pain
C-fibers – small unmyelinated nerve fibers that transmit dull or aching pain.
Three Chronic Pain Conditions
Neuralgia – an extremely painful condition consisting of recurrent episodes of intense shooting or stabbing pain along the course of the nerve.
Causalgia – recurrent episodes of severe burning pain. Phantom limb pain – feelings of pain in a limb that is no
longer there and has no functioning nerves.
Pain Transmission
Acute Pain
Noxious Stimulus travel Via A-Delta and C-delta Fibers to Dorsal Horn (spinal Cord)
Doral HornA-BetaC-Delta
Pain Transmitted to Higher Brain Centers
Acute Pain
STT (Spinal thalamic Tract)
Thalamus and Cortexlocation and discrimination
Retinacular Formation & Periaquductal Gray (PAG)
Motor, sensory and autonomic Response
Discrimination and Location of pain occurs during this sequence
Limbic System& Cortex
Descending Control Mech. Activated here once noxious stimuli reaches higher centers of brain. Incoming stimuli can be inhibited at various levels and endogenous opiates released
Pain Nerve Fibers
Acute Pain Fibers: conduct impulses rapidly. Sharp pain. Restricted area of skin. Seldom continues after stimulation stops.
Chronic Pain Fibers: slower, dull, aching pain. Diffuse and difficult to pinpoint. May continue after stimulus ceases. May be felt in deeper tissues.
An event usually triggers both acute and chronic pain fibers (dual sensation)
Acute Pain
First pain: carried in A-delta fires: larger diameter fibers contain myelin, reflex to get off source, goes to cognitive level (more discrete - very localized)
Second Pain: carried in C fibers. Smaller diameter, non myelinated, slower. (less discrete - more diffuse)
Acute Pain Treatment
Goal– block the pain through:
inhibition blocking A fibers (Gate Control)
Chronic Pain:
Any pain which lasts for six months or more – numerous by-passes. Also goes to limbic
system (emotional control)- learned response
Referred Pain (projected pain)
Felt at other site than injured area– Dermatome (skin represented by nerve root)
Pain theories
Specificity Theory Pattern Theory Gate Control Theory
Specificity theory: specific stimulus has a specific receptor which goes to a location in the brain The specific location identifies the pain’s quality. Thus any noxious stimulus applied to the surface of the skin results in a pain sensation. The evaluation of the type of pain occurs in the brain.
Pattern Theory: a pattern or coding of sensory information is created by different sensations. This theory is faulty due to the number of different types of receptors proven to exist.
Gate Control Theory (1965)
Melzack and Wall originally described a neurophsiologic mechanism which involved the concept of peripheral and central “gating”. The gate theory utilizes the specificity theory and the pattern theory and added the interaction of peripheral afferents with a modulation system in the spinal cord gray matter. Additionally Melzack and Wall believed there also exists a descending modulation system.
Gate Control Theory
First Order neurons: the theory focuses on the first order neurons (primary afferents): the A-beta (large diameter sensory neurons) and A-delta and C neurons (both small diameter sensory neurons).
A nonpainful stimulus can block the transmission of a noxious stimulus
Brain/Pain centersC delta noxious stimulus
A-betanon-painful
stimulusBlocking entry of c-delta Fibers
Gate Control Theory Cont.
The second order neuron, the T-cell and the substantia gelatinosa can exert affects on the primary afferent
Works on the premise that the SG (located in dorsal horn) modulates afferent nerve impulses and influence transmission of T cells. This activates a central controlling mechanism
Gate Control
In Dorsal Horn of Spinal Cord
T
Brain. A-BetaSensory, Proprioception, Etc
A-Delta, C FibersPain Transmission
SG
Facilitator Synapse
Inhibitory Synapse
The second order neuron
When the substantia gelatinosa is active the “gate” is closed and there is a decrease in the amount of sensory input to the T-cell
If the S.G. is relatively inactive the “gate” is open
the balance of activity in the large and small diameter sensory neurons determines the position of the “gate”
Gate Control Theory
Large diameter afferents cause an initial increase in the T-cells followed by a reduction of activity. The initial increase is due to direct activation of the second-order neuron by primary afferents. The reduction is an indirect result due to large-diameter afferents also activating the s.g. cells which causes the gate to close
Gate Control Theory Cont.
Small diameter afferents increase T-cell activity by these primary afferents also activate inhibitory interneurons that reduce activity in the s.g which open the gate
Gate Control Theory
When the balance of small to large diameter sensory neuronal input is no longer maintained and reaches a critical value the second-order neurons are activated. This activation is of the ascending system and leads to the perception of pain and the subsequent behavioral responses.
Gate Control Theory
The Descending control system in which emotion and past experience evoke descending input, impinging upon the gating mechanism to block pain sensation at the spinal level.
PAIN is an excellent “bible” for those working clinically with pain control
Pain modulation: Levels Theory of Pain Control
Spinal Levels of Pain Control– Gate Control Theory– Central Biasing (hyperstimulation analgesia)– Endogenous Opiate (Pituitary level)
Level I: Presynaptic inhibition Gate Control Theory
The concept that when several sensory stimuli reach the spinal cord at the same location and time. one of them becomes dominant.
As long as the stimulation is causing firing of the sensory nerve, the gate to pain should be closed
If accommodation occurs (electrical stimulus) the gate is then open and pain returns
PAIN INHIBITORY COMPLEX: PRESYNAPTIC INHIBITION
PAINRECEPTOR
BRAIN STEM.NEURON
INHIBITORY NEURON
ANTEROLATERALPATHWAY
DORSAL HORN OFSPINAL CORD
+
-
PAIN TRANSMISSION AND INHIBITION
SUBSTANCE P IS THE NEUROTRANSMITTER: BUILDS UP SLOWLY IN THE JUNCTION AND IS SLOWLY DESTROYED
PRESYNAPTIC INHIBITION BY INHIBITORY NEURON BLOCKS THE RELEASE OF SUBSTANCE P (ENKEPHALIN)
Level 2: Descending inhibition
– A theory of pain modulation where higher centers such as the cerebral cortex influence the perception of and response to pain
Impulses from higher centers act to close the gate and block transmission of the pain message at the dorsal horn synapse
Transmission of sensory input to higher brain centers
Transmission Cell
Substantia gelitinosa
A-beta fiber Afferents
A-Delta & Cfiber afferents
CentralControl
+-
+ -
+-
Level 3: -Endorphin modulationEndogenous Opiate
Opiate like substance made by the body Norepinephrine Seratonin
These opiates inhibit the depolarization of second order nociceptive nerve fibers (thus no pain)– Found in substantia gelatinosa - activated in tract– Causes degeneration of prostaglandin and dorsal
horn inhibition
Gate-Control Theory
Brain
Spinal Cord
GatingMechanism
TransmissionCells
Frompainfibers
FromotherPeripheralfibers
Tobrain
Brain
Spinal Cord
GatingMechanism
TransmissionCells
Frompainfibers
FromotherPeripheralfibers
Tobrain
Gate is open Gate is closed
Three Factors Involved in Opening and Closing the Gate
The amount of activity in the pain fibers. The amount of activity in other peripheral
fibers Messages that descend from the brain.
Conditions that Open the Gate
Physical conditions– Extent of injury– Inappropriate activity level
Emotional conditions– Anxiety or worry– Tension– Depression
Mental conditions– Intense concentration or distraction– Involvement and interest in life activities
Types of Pain Medications
Peripherally active analgesics – work at the periphery (e.g., aspirin).
Centrally active analgesics – narcotics that bind to the opiate receptors in the brain (e.g., codeine, morphine, heroin).
Local analgesics – can be injected into the site of injury or applied topically (e.g., novocaine).
Indirectly acting drugs – affect non-pain conditions such as emotions that can exacerbate pain experience.
Psychological Pain Control Methods
Biofeedback – provides biophysiological feedback to patient about some bodily process the patient is unaware of (e.g., forehead muscle tension).
Relaxation – systematic relaxation of the large muscle groups.
Hypnosis – relaxation + suggestion + distraction + altering the meaning of pain.
Psychological Pain Methods
Acupuncture – – Counter-irritation – may close the spinal gating
mechanism in pain perception.
Referred pain
Visceral pain may feel as if it is coming from some part of the body other than the part being stimulated. May arise from common nerve pathways.– Example: Pain originating in the heart may be
referred to the left shoulder and left upper limb.
Pain originating in the heart may feel as if it is coming from the skin because sensory impulses from those two regions follow common nerve pathways to the brain.
Surface regions to which visceral pain may be referred
Theories
A. Convergence theory B. Facilitation theory
Other sensations
Hyperalgesia Itch (pruritus) Vibration sense Two point discrimination Stereognosis
Headaches
Nervous tissue of the brain lacks pain receptors but nearly all other tissues of the head including meninges and blood vessels are richly innervated
Many headaches are associated with stressful life situations that cause fatigue, emotional tension, anxiety, or frustration
Tension Headache
Triggered by various physiological changes such as prolonged contraction of skeletal muscles in forehead, sides of head, back of neck.
Contractions stimulate pain receptors
Vascular Headache
Accompanies constriction or dilation of cranial blood vessels.
Ex. Throbbing headache of “hang-over” from drinking too much alcohol may be due to blood pulsating through dilated cranial vessels
Migraine
Form of vascular headache Certain cranial vessels constrict producing a localized cerebral
blood deficiency Variety of symptoms: seeing patterns of bright light that
obstruct vision, numbness in limbs or face Vasoconstriction subsequently leads to vasodilation of affected
vessels causing severe headache usually on one side of the head.
Can last several hours or more
Other Causes of Headaches
Sensitivity to food additives High blood pressure Increased intracranial pressure due to tumor
or hematoma Decreased cerebrospinal fluid pressure
following lumbar puncture Sensitivity to or withdrawal from certain drugs