05b sensory function
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Neurophysiology Series
SENSORY FUNCTION
OF THE NERVOUS SYSTEMwww.physiology.sdu.edu.cn
By Sawiji AmaniMobile phone: 081 328 028333E-mail: [email protected]
Basic Sciences DepartmentMuhammadiyah Gombong University
Central Java Indonesia
I Sensory pathwaysI Sensory pathways Sensory systems allow us to detect, analyze and
respond to our environment “ascending pathways” Carry information from sensory receptors to the
brain Conscious: reach cerebral cortex Unconscious: do not reach cerebral cortex Sensations from body reach the opposite side of
the brain
1. Sensory receptors1. Sensory receptors
A: Free nerve endings (pain, temperature)
B: Pacinian corpuscle (pressure)
C: Meissner’s corpuscle (touch)
D: Muscle spindle (stretch)
A
B C
D
Sensory receptorsSensory receptors
Ruffini's endings respond to tension and stretch in the skin
Sensory receptorsSensory receptors
Sensory receptors: organs which detect sensory stimuli .
Sensory stimuli: sensation modality (touch, sound, light, pain, cold, and warmth..etc)
Sensory receptorsSensory receptors Mechanoreceptors: detect mechanical compression or
stretching of tissues Thermoreceptors: detect changes in temperature
Nociceptors (pain receptors): detect tissue damage ( physical or chemical damage)
Chemoreceptors: detect taste in the mouth, smell in the nose, oxygen level ..etc.
Electromagnetic receptors (photoreceptor): detect light on the retina
2. Sensory pathways: 3 2. Sensory pathways: 3 neuronsneurons
1st: enters spinal cord from periphery
2nd: crosses over (decussates), ascends in
spinal cord to thalamus
3rd: projects to somatosensory cortex
2.1 Spinothalamic pathway2.1 Spinothalamic pathway
Carries pain, temperature, touch and pressure signals
1st neuron enters spinal cord through dorsal root
2nd neuron crosses over in spinal cord; ascends to thalamus
3rd neuron projects from thalamus to somatosensory cortex
spinothalamicpathway
Spinothalamic Pathway
Small sensory fibres:
Pain, temperature, some touch
Primary somatosensory cortex (S1)
Thalamus
Medulla
Spinal cord
Spinothalamic tract
Spinothalamic damageSpinothalamic damagespinothalamic pathway
Leftspinal cord injury
Loss of sense of:•Touch•Pain•Warmth/coldin right leg
2.2 Dorsal column pathway2.2 Dorsal column pathway
Carries fine touch, vibration and conscious proprioception signals
1st neuron enters spinal cord through dorsal root; ascends to medulla (brain stem)
2nd neuron crosses over in medulla; ascends to thalamus
3rd neuron projects to somatosensory cortex
Two-Point DiscriminationTwo-Point Discrimination
dorsal cloumnpathway
Dorsal column pathwayDorsal column pathway
Large sensory nerves:
Touch, vibration, two-point discrimination, proprioception
Primary somatosensory cortex (S1) in parietal lobe
Thalamus
Medulla
Mediallemniscus
Spinal cord
Dorsal column
Dorsal columnnuclei
Dorsal Dorsal column column damagedamage
dorsal column pathway
Leftspinal cord injury
Loss of sense of:•touch•proprioception•vibrationin left leg
Dorsal column damageDorsal column damage
Sensory ataxia
Patient staggers; cannot perceive position or movement of legs
Visual clues help movement
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint
of Elsevier, Inc. All rights reserved. of Elsevier, Inc. All rights reserved.
ataxia [ah-tak´se-ah] failure of muscular coordination; irregularity of muscular action. adj., adj atac´tic, atax´ic.
sensory ataxia: ataxia due to loss of proprioception (joint position sense), resulting in poorly judged movements and becoming aggravated when the eyes are closed.
Central Pathways
Sensory pathways cross the body’s midline (Silverthorn: 2007)Sensory pathways cross the body’s midline (Silverthorn: 2007)
3.3 Spinocerebellar pathway3.3 Spinocerebellar pathway Carries unconscious propri
oception signals Receptors in muscles & joi
nts 1st neuron: enters spinal cor
d through dorsal root 2nd neuron: ascends to cere
bellum No 3rd neuron to cortex, he
nce unconscious
Spinocerebellar tract damageSpinocerebellar tract damage
Cerebellar ataxia : ataxia due to disease of the cerebellum.
Clumsy movementsIncoordination of the limbs (intention tremo
r)Wide-based, reeling gait (ataxia)Alcoholic intoxication produces similar effe
cts!
4. Somatosensory cortex
Located in the postcentral gyrus of the human cerebral cortex.
Lobus Parietalis: Fungsi & Asosiasi Somatosensoris Gyrus postsentral : korteks somatosensori primer Sentuhan/raba lembut, tekanan, nyeri & suhu, sensasi umum di kepala Sensory ‘homunculus’ (representasi disproporsional)
Spatial orientation of signals.1) Each side of the cortex receives sensory information exclusively from the opposite side of the body
(the exception: the same side of the face).
Spatial orientation of signals.2)The lips, face and thumb are represented by large areas in the somatic cortex,
whereas the trunk and lower part of the body, relatively small area.3)The head in the most lateral portion, and the lower body is presented medially
Sensory ‘homunculus’ (representasi disproporsional)
Sensory ‘homunculus’ (representasi disproporsional)
II . Pain
“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”
International Association for the Study of Pain
Why feel pain?Why feel pain?
Gives conscious awareness of tissue damage
Protection:– Remove body from danger– Promote healing by preventing further damage– Avoid noxious stimuli
Elicits behavioural and emotional responses
free nerve endings in skin respond to noxious stimuli
1. Nociceptors
NociceptorsNociceptorsNociceptors are special receptors that respond only
to noxious stimuli and generate nerve impulses which the brain interprets as "pain".
Adequate Stimulation
–Temperature
–Mechanical damage
–Chemicals (released from damaged tissue)
Bradykinin, serotonin, histamine, K+, acids, acetylcholine, and proteolytic enzymes can excite the chemical type of pain.
Prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them.
Nociopectors
Hyperalgesia:
The skin, joints, or muscles that have already been damaged are unusually sensitive. A light touch to a damaged area may elicit excruciating pain;
Primary hyperalgesia occurs within the area of damaged tissue;
Secondary hyperalgesia occurs within the tissues surrounding a damaged area.
2. Localization of Pain•Superficial Somatic Pain arises from skin areas
•Deep Somatic Pain arises from muscle, joints, tendons & fascia
•Visceral Pain arises from receptors in visceral organs–localized damage (cutting) intestines causes no pain
–diffuse visceral stimulation can be severe•distension of a bile duct from a gallstone
•distension of the ureter from a kidney stone
Most pain sensation is a combination of the two types of message. – If you prick your finger you first feel a sharp pain
which is conducted by the A fibres, – and this is followed by a dull pain conveyed along C
fibres.
3. Fast and Slow Pain
Fast pain (acute)– occurs rapidly after stimuli (.1 second)– sharp pain like needle puncture or cut– not felt in deeper tissues– larger A nerve fibers
Slow pain (chronic)– begins more slowly & increases in intensity– in both superficial and deeper tissues– smaller C nerve fibers
Impulses transmitted to spinal cord by– Myelinated Aδ nerves: fast pain (80 m/s)– Unmyelinated C nerves: slow pain (0.4 m/s)
nociceptor
nociceptor
Aδ nerve C nerve
spinothalamicpathway
to reticularformation
Impulses ascend to somatosensory cortex via:– Spinothalamic pathway (fast pain)– Reticular formation (slow pain)
reticular formation
spinothalamicpathway
thalamus
somato-sensory
cortex
4. Visceral pain
Notable features of visceral pain:Often accompanied by strong autonomic and/or somatic reflexesPoorly localized; may be “referred” referred painMostly caused by distension of hollow organs or ischemia (localized mechanical trauma may be painless)
Afferent innervation of the viscera.Often anatomical separation nociceptive innervation (in sympathetic nerves) from non-nociceptive (predominantly in vagus). Many visceral afferents are specialized nociceptors, as in other tissues small (Ad and C) fibers involved. Large numbers of silent/sleeping nociceptors, awakened by inflammation. Nociceptor sensitization well developed in all visceral nociceptors.
Referred painReferred pain Pain originating from
organs perceived as coming from skin
Site of pain may be distant from organ
Convergence theory: This type of referred pain occurs because both visceral and somatic afferents often converge on the same interneurons in the pain pathways.
Excitation of the somatic afferent fibers is the more usual source of afferent discharge,
so we “refer” the location of visceral receptor activation to the somatic source even though in the case of visceral pain.
The perception is incorrect.
The convergence of nociceptor input from the viscera and the skin.
Referred pain
5. “Pain Gate” Theory5. “Pain Gate” TheoryMelzack & Wall (1965)
A gate, where pain impulses can be “gated”
The synaptic junctions between the peripheral nociceptor fiber and the dorsal horn cells in the spinal cord are the sites of considerable plasticity.
A “gate” can stop pain signals arriving at the spinal cord from being passed to the brain
– Reduced pain sensation– Natural pain relief (analgesia)
descending nerve fibers from brain
axons from touch receptors
axons from nociceptors
“THE PAIN GATE”opioid-releasing interneuron
pain pathways
How does “pain gate” work?How does “pain gate” work?
The gate = spinal cord interneurons that release opioids.
The gate can be activated by:
– Simultaneous activity in other sensory (touch) neurons
– Descending nerve fibers from brain
Applications of pain gateApplications of pain gate
Stimulation of touch fibres for pain relief:– TENS (transcutaneous electrical nerve stimulation)– Acupuncture– Massage
Release of natural opioids– Hypnosis– Natural childbirth techniques
6. Pain Relief6. Pain Relief
Aspirin and ibuprofen block formation of prostaglandins that stimulate nociceptors
Novocain blocks conduction of nerve impulses along pain fibers
Morphine lessen the perception of pain in the brain.
Phantom Limb SensationPhantom Limb Sensation(Tortora & Derrickson, 2006:552)(Tortora & Derrickson, 2006:552)
Patients who have had a limb amputated may still experience sensations such as itching, pressure, tingling, or pain as if the limb were still there.
This phenomenon is called Phantom Limb Sensation.
Why so…?
Some ExplanationsSome Explanations (Tortora & Derrickson, 2006:552)(Tortora & Derrickson, 2006:552)
1. The cerebral cortex interprets impulses arising in the proximal portions of sensory neurons that previously carried impulses from the limb as coming from the nonexistent (phantom) limb.
2. The brain itself contains networks of neurons that generate sensations of body awareness.
3. Neurons in the brain that previously received sensory impulses from the missing limb are still active, giving rise to false sensory perceptions.
(Tortora & Derrickson, 2006:552)(Tortora & Derrickson, 2006:552)
Phantom limb can be very distressing to an amputee.
Many report that the pain is severe or extremely intense, and that it often does not respond to traditional pain medication therapy.
In such cases, alternative treatments may include electrical nerve stimulation, acupuncture, and biofeedback.
Analgesia: Relief from PainAnalgesia: Relief from Pain (Tortora & Derrickson, 2006:553)(Tortora & Derrickson, 2006:553)
Pain sensations sometimes occur out of proportion to minor damage, persist chronically due to an injury, or even appear for no obvious reason.
In such cases, analgesia (an- = without; -algesia = pain) or pain relief is needed.
Analgesic drugs such as aspirin and ibuprofen (for example, Advil or Motrin) block formation of prostaglandins, which stimulate nociceptors.
(Tortora & Derrickson, 2006:553)(Tortora & Derrickson, 2006:553)
Local anesthetics, such as Novocaine, provide short-term pain relief by blocking conduction of nerve impulses along the axons of first-order pain neurons.
Morphine and other opiate drugs alter the quality of pain perception in the brain; pain is still sensed, but it is no longer perceived as being so noxious.
Many pain clinics use anticonvulsant and anti depressant medications to treat those suffering from chronic pain.