Analgesia and relief of pain

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Chapter 32 Analgesia and relief of pain

Chapter contents

Analgesics 248

Principles behind analgesic drugs 250

Specific analgesics 250

Pain is a very necessary sensation as its purpose is to signal harm to an organism. It allows the organism to adapt to its surroundings so that it can remove itself from the sensation or in the case of humans actively resolve the problem by treatment.

All pain receptors are free nerve endings and are called nociceptors. These are part of the process that transmits the pain to the brain (the process of nociception). Various sensory receptors found throughout the body react to a variety of stimuli, such as hot, cold, pressure and chemical, all of which can give the patient the subjective experience of pain. Different types of neuron carry the pain signal to the central nervous system (CNS):

• First-order neurons: transmit pain impulses. There are two subtypes:

• rapidly conducting (12–30 m/s), myelinated A fibres

• slow conducting (0.5–2 m/s) non-myelinated C fibres.

These terminate in the dorsal (posterior) columns of the spinal cord (Figure 32.1).

• Second-order neurons: carry the pain stimuli to the thalamus (Figure 32.2) via the lateral spinothalamic tracts.

Figure 32.1 Anatomy of the spinal cord, showing related sensory and motor areas.

Figure 32.2 Cross-section of the brain and upper spinal cord.

Synapses are formed by both A and C fibres in the dorsal horns (dorsal or posterior columns) of the spinal cord. There is also regulation of the transmission between the nociceptive neurons and those in the spinothalamic tract. Descending fibres from the higher centres can inhibit transmission.

• Third-order neurons go from the thalamus to the cerebral cortex. The thalamus plays a large role in the integration of pain input, whereas the cortical area deals with the meaningful subjective interpretation of pain and can in some cases override the sensation of pain.

The various pain stimuli are:

• Mechanical.

• Chemical: can be triggered chemically at the free nerve ending by changes in the concentration of hydrogen ions (H⁺), serotonin (5-hydroxytryptamine (5-HT)), histamine, bradykinin and eicosanoids (see Figure 32.3, p. 249).

Bradykinin (Figure 32.3) is released when tissue is damaged and so is found in inflammatory processes, e.g. joint inflammation. It stimulates and sensitizes nerve endings, which leads to the stimulus that registers pain with the body. Anti-inflammatories and aspirin inhibit prostaglandin synthesis and therefore the release of mediators that create pain (see Chapter 30 ‘Inflammation and the immune system’, p. 228).

Figure 32.3 Pain stimulants.

Analgesics

Sites of Action

• At the site of injury, by decreasing the pain caused by an inflammatory reaction: aspirin, non-steroidal anti-inflammatories.

• In neurons, to alter the way the nerve conducts: local anaesthetics.

• In synapses in the dorsal horn: opioids and antidepressants.

• At the level of the brain by affecting the perception of pain: opioids and antidepressants.

Terminology

• Analgesia: refers to the specific blocking of the pain receptors, leaving the function of other receptors, such as touch and temperature, intact.

• Anaesthesia: the blocking of all sensations.

Opioid Receptors

• Location

• Substantia gelatinosa (in the dorsal or posterior column) and central grey matter of the brainstem.

• Subgroups

• Mu and kappa receptors: these are responsible for analgesia and respiratory depression.

• Delta receptors: bind endogenous opiates such as enkephalins, endorphins and dynorphins. These are released as neurotransmitters from specific opiate-containing neurons and modify pain sensation. This quality is exploited by morphine-like drugs.

Pain Pathway Transmitters

• Substance P: see Chapter 31 ‘The nervous system’ (p. 235).

• Other opioid peptides: see Chapter 31 ‘The nervous system’ (p. 235).

• 5-HT (serotonin): see Chapter 31 ‘The nervous system’ (p. 235).

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