Allodynia and Hyperalgesia

Allodynia

Allodynia (pain due to a stimulus that does not usually provoke pain). Allodynia is a Greek word for other (allo) pain (dynia). Theoretically, allodynia can be defined as a painful response to a non-nociceptive stimulus i.e. one not encoded by nociceptors, but this definition cannot be used in the clinical setting because it would be impossible to establish whether a stimulus is capable of activating nociceptors in the individual patient.

Types of Allodynia

1.      Static allodynia results from a light touch on the skin.

2.      Dynamic allodynia occurs with movement across the skin.

3.      Thermal allodynia occurs in response to mild changes in temperature.

Allodynia is the result of a pain processing dysfunction in the nervous system called central sensitization. It is not exclusive to migraine, but common in a variety of painful conditions. When allodynia strikes, nerves that carry pain signals react by sending pain signals in response to touch, movement, or temperatures that wouldn’t normally cause pain. It’s an independent symptom that may or may not resolve when the migraine attack subsides. Allodynia is a clinical feature of many painful conditions, such as neuropathies, complex regional pain syndrome, postherpetic neuralgia, fibromyalgia, and migraine. Allodynia may also be caused by some populations of stem cells used to treat nerve damage including spinal cord injury.

Hyperalgesia

Hyperalgesia is increased pain sensitivity (increased pain from a stimulus that usually provokes pain). Hyperalgesia may include both a decrease in threshold and an increase in supra-threshold response. In many cases, it may be difficult to know whether or not the test stimulus is capable of activating nociceptors. Therefore, it is useful to have an umbrella term (hyperalgesia) for all types of increased pain sensitivity. It is often believed that primary hyperalgesia is mainly due to the sensitization of nociceptive nerve endings. Hyperalgesia may not only exist within an area of tissue damage but also in the skin (head zone) remote from the inner organ or muscle which is affected. Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have established that it is possible to experience learned hyperalgesia of the latter, diffuse form.

The focal form is typically associated with injury, and is divided into two subtypes:

1.      Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues.

2.      Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues.

Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This seems to occur via immune cells interacting with the peripheral nervous system and releasing pain-producing chemicals (cytokines and chemokines). Stimulation of nociceptive fibres in a pattern consistent with that from inflammation switches on a form of amplification in the spinal cord, long term potentiation. This occurs where the pain fibres synapse to the pain pathway, the periaqueductal grey. Amplification in the spinal cord may be another way of producing hyperalgesia.

Hyperalgesia and allodynia are classified according to the type of stimulus which elicits the sensation of pain. Thermal (heat or cold) stimuli or mechanical brush, pinch, or pressure stimuli are most often used. In addition, moving (dynamic) or static mechanical touch stimuli are being used. Thereby, mechanical and thermal (heat or cold) hyperalgesia and mechanical dynamic allodynia can be differentiated.