The hyperalgesia it is a phenomenon characterized by developing a state of increased sensitivity to pain. This condition occurs after an injury and may consist of a chronic alteration.
The main feature of hyperalgesia is the development of excessive sensitivity to pain. People who suffer from this phenomenon have a very low pain threshold, so any stimulus, no matter how small, can generate very intense painful sensations.
Hyperalgesia is a highly frequent symptom in many forms of neuropathic pain and is generated mainly due to a traumatic or inflammatory lesion of the skin.
This phenomenon can develop in two concentric areas: in the region immediately surrounding the injury (primary hyperalgesia) and in the area that extends beyond the point of injury (secondary hyperalgesia).
The treatment of this condition is usually subject to the intervention of the pathology that causes the traumatic or inflammatory lesion of the skin. However, in several cases hyperalgesia tends to become chronic and irreversible.
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Hyperalgesia is a symptom that is usually very prevalent in different cases of neuropathic pain. The main characteristic of this phenomenon is to experience a high sensitivity to pain.
As the main result of this condition, the person experiences an abnormal and excessive response to pain. That is, it is much less resistant to painful stimuli and, elements that are usually innocuous, are perceived with high sensations of pain.
Likewise, people with hyperalgesia have very little resistance to normal pain processes. In other words, painful stimuli that are unpleasant for most people can be experienced in an extremely intense and unbearable way by individuals with this type of condition..
In this sense, several studies suggest that hyperalgesia not only constitutes a quantitative sensory change, but also constitutes a qualitative modification in the nature of sensations.
Specifically, the sensations evoked by stimulation of the peripheral tissues of the body are perceived in a totally different way by people with hyperalgesia. This fact translates into high pain responses to any type of stimulus.
Research on hyperalgesia suggests that most of this manifestation is due to alterations in the properties of the “healthy” primary afferent pathways that remain between damaged afferent fibers..
However, certain studies point out that, in people with neuropathic pain, hyperalgesia is a condition that is maintained by the ectopic activity generated in the damaged nerves.
Finally, hyperalgesia is characterized by incorporating a component known as allodynia. This element refers to pain evoked by touch and is produced by variations in the central processing of signals generated in lowered threshold mechanoreceptors.
All these data have postulated the hypothesis that hyperalgesia caused by peripheral nerve injuries depends mainly on alterations in the central nervous system..
These brain alterations would be caused directly by the damaged afferent tracts and would result in the typical symptom of hyperalgesia: increased sensitivity to pain.
Hyperalgesia is a phenomenon that develops mainly through alterations in the central nervous system. That is, modifications in brain function result in increased sensitivity to pain..
Likewise, research indicates that for alterations of the central nervous system to generate hyperalgesia, it is necessary that these alterations are maintained by ectopic or evoked activity.
However, to correctly understand the biological bases of hyperalgesia, it is necessary to take into account that, although this phenomenon depends mainly on the functioning of the central nervous system, its origin or initial damage is not located in this region of the body..
In fact, hyperalgesia is a phenomenon that does not originate as a consequence of direct damage to the brain, but rather to the afferent fibers that travel from the spinal cord to the brain..
As a consequence of the damage to the primary afferent fibers, irritation of the cells of the nervous system occurs. This irritation causes physical changes in the damaged tissue and causes intense and repeated stimuli of inflammation..
This fact causes the threshold of nociceptors (brain pain receptors) to decrease, so stimuli that previously did not cause pain now do cause it.
More specifically, it has been shown that the irritation and / or damage caused by hyperalgesia can involve both the nociceptor itself and the nerve fiber corresponding to the first sensory neuron..
For this reason, it is currently held that hyperalgesia is a phenomenon that can be caused by both specific damage to the central nervous system and the peripheral nervous system (or both)..
In this sense, the biological basis of this phenomenon lies in two main processes:
This fact causes that the information that travels from one side to another (from the spinal cord to the brain) does not respond to the original damage itself, but to the altered properties generated by the central nervous system about the perceived stimulus..
The manifestations of hyperalgesia can vary in each case. In fact, sometimes, hypersensitivity to pain can be higher than in other cases.
In this sense, two main types of hyperalgesia have been described: primary hyperalgesia (increased sensitivity to pain in the injured region) and secondary hyperalgesia (increased sensitivity to pain in adjacent uninjured sites).
Primary hyperalgesia is characterized by the experience of an increased sensitivity to pain in the same site where the injury has occurred. This condition is directly related to the peripheral release of harmful intracellular or humoral mediators.
Primary hyperalgesia corresponds to the first level of neuropathic pain. Characterized by manifestations of peripheral sensitization, but central sensitization has not yet been established.
At a therapeutic level, the suffering of this type of hyperalgesia determines an alarm signal to apply more aggressive and effective analgesic techniques and, in this way, avoid the development towards phases of worse prognosis.
Secondary hyperalgesia establishes a type of increased sensitivity to pain in regions adjacent to the injured area. In this case, hyperalgesia usually extends to the dermatomes, both above and below the area where the injury has occurred..
This type of condition is usually associated with spasms and immobility ipsilateral (on the same side of the body where the injury is located) or contralateral (on the opposite side of the body where the injury has occurred).
Likewise, secondary hyperalgesia usually generates changes in the excitability of neurons in the spinal cord and supra-medullary. Several studies show that this condition would be the expression of the association to the phenomenon of central sensitization.
Hyperalgesia is considered a pathognomic symptom of neuropathic pain, since most cases of this phenomenon tend to present in conjunction with the rest of the symptoms of the disease..
Likewise, another interesting line of research about increased sensitivity to pain is constituted by a condition known as hyperalgesia associated with opioid treatment..
Neuropathic pain is a disease that affects the somatosensory system of the brain. This condition is characterized by the development of abnormal sensations such as dysesthesia, hyperalgesia, or allodynia..
Thus, the main characteristic of neuropathic pain is to experience continuous and / or episodic components of painful sensations..
This condition originates from an injury to the spinal cord, which can be caused by conditions such as multiple sclerosis, strokes, some cases of diabetes (diabetic neuropathy), and other metabolic conditions..
On the other hand, herpes zoster, nutritional deficiencies, toxins, distant manifestations of malignant tumors, immune disorders and physical trauma to the nerve trunk are other types of factors that can cause neuropathic pain and, therefore, hyperalgesia.
Hyperalgesia associated with opioid treatment or induced by opioids constitutes a paradoxical reaction characterized by an intensified perception of pain related to the use of these drugs (Gil, A. 2014)..
In these cases, the increased sensitivity to pain is directly related to the effect of these substances at the brain level..
This condition has been observed in both patients receiving maintenance doses of opioids, as well as in patients who are withdrawn from these drugs and patients who consume high doses of these types of drugs..
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