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Physiology of pain

Physiology 7-Pain

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Page 1: Physiology 7-Pain

Physiology of pain

Page 2: Physiology 7-Pain

Pain • unpleasant sensory & emotional

feeling, connected with true or potential damage of tissue or organ, which is described in the terms of such a damage.

International expert commiteeJ. “Pain” 6, 248-252, 1979

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Pain • Doesn’t give any info about the external

environment;• Adequate stimulus – any suprathreshold

stimulus damaging the tissue or causing the danger of damage:

MechanicalThermal (burn or frostbite)Chemical (metabolism disorders)

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pain• Danger signal that occurs at the damage

or the threat of damage of:SkinPeritoneumMeninxPericardithis.

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Nociception • Nociception - sensor modality in

animals which causes pain feeling in man.

• Nociceptors - pain receptors

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Types of painPain

Somatic Visceral

superficial deep

Early or primaryepicritical

Delayed or secondaryprotopatic

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Superficial pain localization - skin

Early or primary – strictly localized,

Dissapears with the dissapearence of the stimulus

(pinch, hit, pin)

Latent period – sec

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Superficial pain localization - skin

Delayed or secondary- Not localized, dyes out

slowly.Dull, diffuse

Latent period – 0,5-1,0 sec

diffuse

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Deep painLocalization - connective tissue, muscles, bones, joints, teethTypes – muscle cramps, headache, toothache. Characteristics - dull, non-localized,irradiating Latent period 1-3 minAcute, sub-active, chronic

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Visceral pain

Diffuse pain Pain with irradiation

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Visceral pain• Localization – internal organs• Types - kidney, liver, intestinal cramps,

gastric ulcer pains, appendicitis, cardiac pain • Characteristics - dull, non-localized,

irradiating to other organs & tissue. May be acute but diffuse.

• Reasons – quick & excessive stretching of hollow organs, cramps, spastic contractions, ischemia

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Pain duration• Acute pain – localized in the damaged area, its

intensity depends on the stimulus intensity, has signaling function, quickly dissapears.

• Chronic pain – lasts up till half a year, has stable & recurrent forms. No connections between pain intensity & level of organic damage.

• May become a separate syndrome

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Other types of pain• Psycogenic – no peripheral organic

reason – neurosis.• Itching – caused by the increased

concentration of hystamine in skin

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COMPONENTS OF PAIN

1. SENSORY DISCRIMINATIVE2. AFFECTIVE (EMOTIONAL)3. VEGETATIVE4. LOCOMOTOR5. COGNITIVE (intensity evaluation)

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SENSORY DISCRIMINATIVE• Is enabled by thalamus & cortex.• When the hand is deepened into the water with

t0>450С skin receptors are excited, they send info to the cortex about the localization of hot stimulus, its intensity, the starting point & the end point of its action.

• Sensation is formed• This component prevails in superficial pain

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Affective or emotional• Is enabled by limbic system• Negative emotions are formed• Is the prevailing component in chronic pain

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vegetative• Is enabled by ANS• BP elevation, HR increase, pupil dilation,

changed rhythm of respiration • Sympatho-adrenal system is activated,

vasopressin (АDH) is produced.• Is the strongest in visceral pain

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locomotor

• Is enabled by motor zones of cortex• Is displayed in flexor reflexes (defence

reflex), abdominal muscles tension, pscycomotor behavioral reactions

• Accompanies all types of pains

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cognitive• Present pain is evaluated in comparison to

previous pains.• This evaluation depends on many factors:Social statusBringing up in the familyEthnic originCircumstances at which the pain occured

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Pain neurophysiology

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Pain theories

1. Theory of specificity – M.Frey – end of XIX century

2. Theory of intensity – Goldshteiner - end of XIX century

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Theory of specificity

• Pain is an independent feeling with specialized nervous apparatus of receptors, conducting pathways & centres

• Prof – the correlation between skin pain dots and the dots of pressure & temperature is 9:1

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Pressure & pain dots on the skin

Pressure dot

Pain dots

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Intensity theory

• Pain may be caused by suprathreshold stimuli of different modality.

• Not proved to be true.

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NociceptorsFree nervous endings of 2 types:• Non-myelinized fibres of C type – the velocity

of impulse conduction is up to 1 m/sec – are present everywhere (skin, joints, internal organs)

• Myelinized fibres of Аδ type – the velocity of impulse conduction is up to 20

m/sec– only in skin

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Nociceptors Аδ • High threshold receptors;• May be sencibilized ;• Have small receptive fields.• 3 types:Mechano-Тhermo-Mechano-thermo-

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Nociceptors of С type fibres

• High threshold, may cause sencibilization, have big receptive fields (17mm2).

• Polymodal

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Nociceptors blocking

• Local anaestetics in low concentration block С type fibres

• Pressure – blocks just Аδ fibres. This activates С fibres

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Algogenic substanses• Substances from damaged cells – potassium,,

АТP. • From plasma – bradikinins, Н+

• From must cells – hystamine• From platelets – serotonin• From nervous afferent fibres – substance Р• SNS mediators – adrenalin,noradrenalin

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Nociceptive system

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Receptive fields

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Spinal cordЖелатинозная субстанция

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skin

Internal org.

Аδ

Аδ

С

С

С

n. Vagus 70%

VPLThalamus

SI-SII

Thalamusn.medialis

5 –Associative cortex.(temporal & frontal)RF

3

45

12

1 –Tr. Neospino-thalamicus2 – tr. Paleospinothalamicus3 – Hypothalamus4 – Limbic cortex

Asparaginic acid

Sub. Р

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Conducting pathways• Tr. Neospino-thalamicus – in the anterior

funiculus, has somatotypical organization. Enables primary pain conduction.

• Tr. paleospinothalamicus – non-specific system (RF) – has many synapses on one level in the spinal cord, makes diffuse connections in cortex. Enables emotional component of pain – secondary pain

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First danger (bacterial infection, inflamation, mechanical influence)

Cortex- feeling of pain

Afferent fibres

Spinal cord

Supraspinal centers

Impulse conduction

Transduction & transformation

Nociceptors

Algogenic substanses formation

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Refered pains

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Pain irradiation

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Pain progection in the cortex (due to lateral spino-thalamicus tract)

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Antinociceptive systemGigantic-cell nucleus RF

Spinal cord neurons secreting endoopiates

Inhibition of afferent nociceptive neurons & neurons of posterior horn ІІ & Y plates

serotonin

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Antinociceptive systemCentral grey matter

Ruph nucleiNoradrenalin, alpha-2 adrenoreceptors

serotonin

Spinal cord neurons releasing endoopiates

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OPIOID ANALGESICS• Relieve pain as a symptom• Perception of pain & reaction to it are both

altered• Opioid receptor activation reduces intracellular

c-AMP formation,opens K-channels or suppresses voltage-gated Ca- channels, hyperpolarization of a neuron, decreased neurotransmitter release by CNS & myenteric neurons

Page 46: Physiology 7-Pain

MECHANISM OF OPIOID ACTION