Nociception and Peripheral Sensitisation

Nociceptive pain

Pain associated with tissue injury or damage, even potential damage

7 clinical criteria (3 criteria for presence of symptoms in the case of the absence of 4 criteria)

1. Localised pain to the area of injury/Recent onset

2. Clear proportional mechanical/anatomical nature to aggravating and easing factors

3. Usually intermittent and sharp with movement or mechanical provocation but otherwise can be a dull constant ache or throb at rest.

Area of pain, Predictable Aggs+Eases, Sensation=APAES=

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IN THE ABSENCE OF

1. Pain in association with dysesthesias

2. Night pain/disturbed sleep

3. Antalgic posture/movements

4. Sharp, shooting or burning type pain

DNDAMNTP

Ducks Never Do A Misdeed, No They’re Perfect

Dysesthsia, Night Disturbance, Antalgic Movements, Neuropathic Type Pain

The 4 phases of nociception

1. Transduciton

2. Transmission

3. Modulation

4. Perception

TTMP

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Transduction

• Nociceptors transducer and encode noxious stimuli (thermal, mechanical, chemical)

Types of Nociceptors (3)

1. Mechanical

2. Thermal

3. Chemical

Location of Nociceptors

• Found in the skin at veryin densities based on location eg more in fingertips, hands, and face, but less over the torso

• Can be internal and are within muscles, joints, bones, and internal organs

Types of axons involved in nociception

A-Alpha fibres

A-Beta fibres

A-Delta fibres

C fibres

A-alpha + A-beta fibres

• myelinated

• Large diameter

• Pick up light touch, and are proprioceptive

A-delta fibres

• Lightly myelinated

• Medium diameter

• Nociceptive

  • Small, fast, and well localised pain - these fibres are responsible for the initial pain feeling

C fibres

• Unmyelinated

• Small diameter

• Nociceptive

  • Slow and poorly localised pain - responsible for th elating, dull, throbbing feeling

Peripheral Sensitisation process

• stimulus leads to opening of ion channels in nociceptor, allowing them to reach threshold to create an action potential

• Nociceptor sensitising mediators are produced during peripheral inflammation by injured tissue and immune cells

• These sensitising mediators reduce the threshold of the receptors so that the pain response is generated from less input, to prevent further injury to the tissue and allow for healing

Substances involved in peripheral sensitisation

• Chemical mediators of inflammation - Histamine, Bradykinin, Prostaglandins

• Neuropeptides - Supstance P, Chemokines, Cytokines

Peripheral sensitisation definition

An increases responsiveness and reduced threshold of nociceptors to stimulation in their receptive fields

• peripheral sensitisation only occurs at sites on ongoing inflammation

What way and along what tract does pain ascend

Pain ascends contra-laterally and along the Spino-Thalmic Tract

Transmission via the Spinothalmic Tract

• Nociceptors detect and transduce the noxious stimulus

• A-delta and C fibres carry the action potential along the 1st order neuron to the spinal cord and substantia gelatinosa

• A synapse occurs in the substantia gelatinosa between the 1st and 2nd Order neuron, and this is where Substance P and Glutamate are released.

• The 2nd order neuron decussates here in the spinal cord, crossing over to the contralateral side, and ascends via the spinothalmic tract to the thalamus.

• At the thalamus, the signal is relayed to the somatosensory cortex via a synapse between the 2nd and 3rd order neuron

Noxious Stimulus definition

An actually or potentially tissue damaging stimulus

Nociception

The neural process of encoding and processing noxious stimuli

Sensitisation

Increased responsiveness to neurons to their normal input or recruitment of a response to the normally subthreshold inputs

Central sensitisation

Increased responsiveness of Nociceptive neurons in the central nervous system to their normal or subthreshold afferent input